Miracle-dz/UniFAR-FTUs huggingface dataset:
The role of Plo1 kinase in mitotic commitment and septation in Schizosaccharomyces pombe

Plo1‐associated casein kinase activity peaked during mitosis before septation. Phosphatase treatment abolished this activity. Mitotic Plo1 activation had a requirement for prior activation of M‐phase promoting factor (MPF), suggesting that Plo1 does not act as a mitotic trigger kinase to initiate MPF activation during mitotic commitment. A link between Plo1 and the septum initiating network (SIN) has been suggested by the inability of plo1Δ cells to septate and the prolific septation following plo1+ overexpression. Interphase activation of Spg1, the G protein that modulates SIN activity, induced septation but did not stimulate Plo1‐associated kinase activity. Conversely, SIN inactivation did not affect the mitotic stimulation of Plo1‐associated kinase activity. plo1.ts4 cells formed a misshapen actin ring, but rarely septated at 36°C. Forced activation of Spg1 enabled plo1.ts4 mutant cells, but not cells with defects in the SIN component Sid2, to convert the actin ring to a septum. The ability of plo1+ overexpression to induce septation was severely compromised by SIN inactivation. We propose that Plo1 acts before the SIN to control septation.
Some aspects of the use of laser Doppler flow meters for recording tissue blood flow

Laser Doppler flow meters are used to provide continuous records of blood flow in tissues. An account is given of their principles of operation and of the differences between two of the commercially available instruments: the Periflux model PF3 and the Moor blood flow monitor model MBF3D. The Periflux tended to have higher noise levels and to drift more than the Moor. The principal disadvantage of these instruments is that they cannot be calibrated in absolute units of blood flow. It is suggested that the method of standardization adopted for the Periflux be used with other machines, based on the signal produced by the Brownian motion of a 0.5% suspension of 0.48 micron diameter polystyrene microspheres at 20 degrees C. The signal representing zero flow in a tissue can be obtained by recording with the same light intensity from a stationary reflector. In model systems the instruments are linear with red cell volume fractions up to only 1%, which is below that likely to be encountered in many tissues. The effects of ambient light and the origin of movement artifacts are also considered.
Analysis of coupling strength in multi-domain magneto-systems

Summary form only given. In recent years, novel devices which use nanomagnets to store and transmit information have been a particular topic of interest. Many of these devices utilize dipolar coupling between nanomagnets to process or communicate information and the most important factor when designing these systems is knowing if two nanomagnets are perfectly coupled [1]. However, when modeling these devices, these nanomagnets are typically modeled as single-domain objects even though in many cases, the magnet dimensions far exceed the exchange length [2]. While it is expected that very small magnets can be treated as single-domain objects, it is not quite clear how small is small enough. Second, it is not clear whether using a single-domain analysis underestimates or overestimates the coupling. In this work, we quantify the coupling between nanomagnets while considering their multi-domain behavior. Our simulations conclusively prove that ignoring multi-domain effects beyond a certain size yields inaccurate results. While the single-domain assumption predicts similar coupling strength to the multi-domain models for thin-film magnets with areas smaller than 1 μm2, the two models disagree about the coupling strength between larger magnets.
I Models and Tools for the Dynamic Reconfiguration of FPGAs

This tutorial outline summarizes the tools and the methods that are used to bridge the design gap between the specification of a dynamically reconfigurable application and its implementation in a FPGA system. The tools and methods used when designing dynamically reconfigurable systems are influenced by the target application domain. In this tutorial, it is assumed that the application is an embedded processor system implemented in a single platform FPGA. Dynamic reconfiguration will be used to time-multiplex mutually exclusive sub-components in the system architecture that are used periodically. Simulating dynamically reconfigurable systems in RTL simulators has been investigated but RTL simulators normally do not allow the topology of the system architecture to change during simulation. 'Virtual multiplexors', placed at subcomponent I/O interfaces, determine which sub-component receives input and generates output. A reconfiguration controller switches the virtual multiplexors according to a given reconfiguration schedule or algorithm. The design of a dynamical and partial hardware reconfigurable system is however still not sufficient supported by design tools. To accomplish this, the signal lines for communication with the functionality in the reconfigurable area must be placed at a known position, which can be done by using so called macros
Effects of Resveratrol on Inflammation and Apoptosis After Experimental Spinal Cord Injury.

AIM To determine the effects of resveratrol on inflammation and apoptosis after experimental spinal cord injury (SCI). MATERIAL AND METHODS Eighteen Sprague-Dawley rats were randomly divided into three groups. All groups underwent thoracic laminectomy. The first group received no other intervention. The second and third groups suffered SCI via the aneurysm clip compression method, and additionally the third group received resveratrol. After euthanizing the rats, immunohistochemical analysis and biochemical parameters of tumor necrosis factor alpha (TNF-? ) and interleukin (IL)-1? were measured. RESULTS The resveratrol group had statistically significant lower levels of TNF-? , IL -1? , and terminal deoxynucleotidyl transferasemediated dUTP nick-end labeling (TUNEL) positive cells and higher number of glial and motor neuron cells. CONCLUSION Resveratrol proves to have remarkable neuroprotective effects on SCI in an experimental model in addition to its proven cardioprotective effects.
Slaves Citizens Sons Legal Metaphors In The Epistles

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Supervoxel Plane Segmentation and Multi-Contact Motion Generation for Humanoid Stair Climbing

Stair climbing is still a challenging task for humanoid robots, especially in unknown environments. In this paper, we address this problem from perception to execution. Our first contribution is a real-time plane-segment estimation method using Lidar data without prior models of the staircase. We then integrate this solution with humanoid motion planning. Our second contribution is a stair-climbing motion generator where estimated plane segments are used to compute footholds and stability polygons. We evaluate our method on various staircases. We also demonstrate the feasibility of the generated trajectories in a real-life experiment with the humanoid robot HRP-4.
Block-Based Quantized Histogram (BBQH) for efficient background modeling and foreground extraction in video

This paper proposes an efficient way of background modeling and elimination for extracting foreground information from the video, applying a new block-based statistical feature extraction technique coined as Block Based Quantized Histogram (BBQH) for background modeling. The inclusion of contrast normalization and anisotropic smoothing in the preprocessing step, makes the feature extraction procedure more robust towards several unorthodox situations like illumination change, dynamic background, bootstrapping, noisy video and camouflaged conditions. The experimental results on the benchmark video frames clearly demonstrate that BBQH has successfully extracted the foreground information despite the various irregularities. BBQH also gives the best F-measure values for most of the benchmark videos in comparison with the other state of the art methods, and hence its novelty is well justified.
Biosynthesis and biochemical properties of the hepatitis C virus core protein

The biosynthesis and biochemical properties of the putative nucleocapsid protein of hepatitis C virus (HCV) were investigated. RNA transcripts for cell-free translation were prepared from truncated form of the cDNA construct encoding the structural proteins of HCV. Processing of the translation products was dependent on microsomal membranes and signal recognition particle, suggesting that release of the 21-kDa core protein from the polyprotein precursor is mediated solely by the signal peptidase of the endoplasmic reticulum (ER) and is achieved by the removal of a putative signal sequence of approximately 18 residues located at its C terminus. The core protein was found to bind membranes in vitro and in transfected cells, as shown by centrifugation analysis of in vitro translation products and transfected-cell lysates. Immunofluorescence of transfected cells showed that the core protein colocalized with the E2 glycoprotein as well as with a cellular ER membrane marker. The nucleocapsid protein expressed by in vitro translation in rabbit reticulocyte lysates cosedimented with the large ribosomal subunit in sucrose gradients. The ribosome binding domain was mapped to the N-terminal region of the core protein. Moreover, the same region was shown to bind RNA in vitro, suggesting that cosedimentation of core protein with ribosomes may be mediated by the RNA binding of the nucleocapsid protein of HCV. These studies indicate that the HCV core protein is a cytoplasmic protein associated with the ER membranes and possesses RNA binding activity.
Combining xenon and mild therapeutic hypothermia preserves neurological function after prolonged cardiac arrest in pigs*

Objective:Despite the introduction of mild therapeutic hypothermia into postcardiac arrest care, cerebral and myocardial injuries represent the limiting factors for survival after cardiac arrest. Administering xenon may confer an additional neuroprotective effect after successful cardiopulmonary resuscitation due to its ability to stabilize cellular calcium homeostasis via N-methyl-D-aspartate-receptor antagonism. Design:In a porcine model, we evaluated effects of xenon treatment in addition to therapeutic hypothermia on neuropathologic and functional outcomes after cardiopulmonary resuscitation. Setting:Prospective, randomized, laboratory animal study. Subjects:Fifteen male pigs. Interventions:Following 10 mins of cardiac arrest and 6 mins of cardiopulmonary resuscitation, ten pigs were randomized to receive either mild therapeutic hypothermia (33°C for 16 hrs) or mild therapeutic hypothermia 1 xenon (70% for 1 hr). Five animals served as normothermic controls. Measurements and Main Results:Gross hemodynamic variables were measured using right-heart catheterization. Neurocognitive performance was evaluated for 5 days after cardiopulmonary resuscitation using a neurologic deficit score before the brains were harvested for histopathological analysis. All animals survived the observation period in the mild therapeutic hypothermia 1 xenon group while one animal in each of the other two groups died. Mild therapeutic hypothermia 1 xenon preserved cardiac output during the induction of mild therapeutic hypothermia significantly better than did mild therapeutic hypothermia alone (4.6 6 0.6 L/min vs. 3.2 6 1.6 L/min, p # .05). Both treatment groups showed significantly fewer necrotic lesions in the cerebral cortex, caudate nucleus, putamen, and in hippocampal sectors CA1 and CA3/4. However, only the combination of mild therapeutic hypothermia and xenon resulted in reduced astrogliosis in the CA1 sector and diminished microgliosis and perivascular inflammation in the putamen. Clinically, only the mild therapeutic hypothermia 1 xenon-treated animals showed significantly improved neurologic deficit scores over time (day 1 = 59.0 6 27.0 vs. day 5 = 4.0 6 5.5, p ø .05) as well as in comparison to the untreated controls on days 3 through 5 after cardiopulmonary resuscitation. Conclusions:These results demonstrate that even a short exposure to xenon during induction of mild therapeutic hypothermia results in significant improvements in functional recovery and ameliorated myocardial dysfunction. (Crit Care Med 2012; 40:–1303)
Effects of an antistroke agent MCl-186 on cerebral arachidonate cascade.

Activation of the cerebral arachidonate (AA) cascade is one of the major causes of edema and tissue injury in cerebral ischemia, particularly after reperfusion. The cascade produces toxic oxygen radicals responsible for peroxidative neurodegeneration and synthesizes, the potent edematous inducer, leukotrienes. The present study was undertaken to evaluate the effect of MCl-186 (3-methyl-1-phenyl-pyrazolin-5-one), a radical scavenger and antioxidant which has beneficial anti-ischemic actions, on the cerebral AA cascade. Postischemic treatment with MCl-186 (1.0 and 3.0 mg/kg i.v.) significantly inhibited the aggravation of cortical edema seen 60 min after recirculation following 30 min of ischemia in gerbils. An antilipoxygenase agent, FPL-55712 (7-[3-(4-acetyl-3-hydroxy-2-propylphenoxy)-2- hydroxypropoxy]-4-oxo-8-propyl-4H-1-benzopyran-2-carboxylic acid, monosodium salt; 10 mg/kg i.v. ) or AA-861 ((2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinon e; 60 mg/kg i.p.) was also effective in this model; however, indomethacin (4 mg/kg i.p.), a cyclooxygenase inhibitor, was ineffective. Concomitant treatment with MCl-186 (0.1-3.0 mg/kg i.v.) remarkably inhibited the swelling observed 24 hr after cortical infusion of AA (80 micrograms) in rats. Similarly, antilipoxygenase agents clearly inhibited the AA-induced edema. Furthermore, postischemic treatment with MCl-186 (0.3-3.0 mg/kg i.v.) inhibited the facilitation of cerebral leukotriene synthesis seen 15 min after recirculation following 30 min of ischemia in gerbils. These findings suggest that the site of action of MCl-186 as an anti-ischemic agent may be closely associated with the cerebral AA cascade, especially the lipoxygenase system, activated by ischemia-reperfusion.
Stat1 Negatively Regulates Immune-Mediated Injury with Anaplasma phagocytophilum Infection

Human granulocytic anaplasmosis (HGA) is caused by the obligate intracellular bacterium Anaplasma phagocytophilum. Our data previously demonstrated that A. phagocytophilum induces an immunopathologic response by activating IFN-γ production through the Stat1 signaling pathway. In this study, we investigated the broader role of Stat1 signaling in the host response to infection with A. phagocytophilum. In Stat1 knockout (KO) compared with wild-type mice, A. phagocytophilum infection was more highly pathogenic as characterized by the unanticipated development of clinical signs in mice including markedly increased splenomegaly, more severe inflammatory splenic and hepatic histopathology, >100-fold higher blood and splenic bacterial loads, and more elevated proinflammatory cytokine/chemokine responses in serum. CD4+ and CD8+ T lymphocyte populations were significantly expanded in spleens of A. phagocytophilum–infected Stat1 KO mice compared with wild-type mice. The leukocyte infiltrates in the livers and spleens of A. phagocytophilum–infected Stat1 KO mice also contained expansions in neutrophil and monocyte/macrophage populations. Importantly, A. phagocytophilum–infected Stat1 KO mice did not demonstrate induction of inducible NO synthase in splenocytes. These results show that Stat1 plays an important role in controlling bacterial loads but also by unexpectedly providing an undefined mechanism for dampening of the immunopathologic response observed with A. phagocytophilum infection.
A regression model with ARIMA errors to investigate the frequency and severity of road traffic accidents.

In this paper, models are developed to explain and forecast the frequency and severity of accidents in Belgium. The objective of this study is to enhance the understanding of the developments in road safety by studying the impact of various explanatory variables on traffic safety. It is investigated whether the number of accidents and victims is influenced by weather conditions, economic conditions and policy regulations. The model is used to predict the frequency and severity of accidents for a 12-months out-of-sample data set. Monthly Belgian data from January 1974 to December 1999 are used in the model, and predictions are made for the year 2000. Using a regression model with ARIMA errors, the impact of variables on aggregate traffic safety is quantified and at the same time the influence of unknown factors is captured by the error term. The results show a significant effect of weather conditions and laws and regulations on traffic safety, but there seems to be negligible statistical impact of economic conditions. The model can easily be used to forecast traffic safety, as can be seen from the reasonably good fit obtained on a 95% confidence level. (Author/publisher)
The Inositol 1,4,5-Trisphosphate Receptor (IP3R) and Its Regulators: Sometimes Good and Sometimes Bad Teamwork

In both nonexcitable and excitable cells, the inositol 1,4,5-trisphosphate receptor (IP3R) is the primary cytosolic target responsible for the initiation of intracellular calcium (Ca2+) signaling. To fulfill this function, the IP3R depends on interaction with accessory subunits and regulatory proteins. These include proteins that reside in the lumen of the endoplasmic reticulum (ER), such as chromogranin A and B and ERp44, and cytosolic proteins, such as neuronal Ca2+ sensor 1, huntingtin, cytochrome c, IP3R-binding protein released with inositol 1,4,5-trisphosphate, Homer, and 4.1N. Specific interactions between these modulatory proteins and the IP3R have been described, making it clear that the controlled modulation of the IP3R by its binding partners is necessary for physiological cell regulation. The functional coupling of these modulators with the IP3R can control apoptosis, intracellular pH, the initiation and regulation of neuronal Ca2+ signaling, exocytosis, and gene expression. The pathophysiological relevance of IP3R modulation is apparent when the functional interaction of these proteins is enhanced or abolished by mutation or overexpression. The subsequent deregulation of the IP3R leads to pathological changes in Ca2+ signaling, signal initiation, the amplitude and frequency of Ca2+ signals, and the duration of the Ca2+ elevation. Consequences of this deregulation include abnormal growth and apoptosis. Complex regulation of Ca2+ signaling is required for the cell to live and function, and this difficult task can only be managed when the IP3R teams up and acts properly with its numerous binding partners. Changes in the amount of calcium inside cells initiate many cellular events, including muscle contraction, hormone secretion, and cell growth. These changes can be modulated in time and space by the cell to tailor its response to the prevailing conditions. A major pathway used for the release of calcium from intracellular stores involves opening the inositol 1,4,5-trisphosphate receptor (IP3R), a calcium channel that is part of a signaling complex with multiple binding partners. This Review, which contains 2 tables, 6 figures, and 119 references, discusses the role of specific binding partners in regulating the function of the IP3R. These studies provide information on how these channels work and form the background for the investigation of disease-induced changes in calcium release channel function. The initiation of intracellular calcium signals can depend on factors as diverse as the nonuniform distribution of a binding partner in the lumen of the endoplasmic reticulum or the activation of a calcium-binding protein in the cytoplasm. Once calcium signals start, they can be transient, sustained, or oscillating; these temporal aspects of the signal are regulated by similarly diverse factors. Changes in intracellular calcium regulation occur in many diseases. As more and more new regulators of the IP3R are discovered, it will be important to understand the teamwork needed to regulate and modulate this complex system.
Pharmacological characterization of FK1052, a dihydropyridoindole derivative, as a new serotonin 3 and 4 dual receptor antagonist.

(+)-8,9-Dihydro-10-dihydro-10-methyl-7-[(5-methyl-4-imidazolyl) methyl]pyrido-[1,2-a]indol-6(7H)-one hydrochloride (FK1052) is a newly designed and synthesized 5-hydroxytryptamine (5-HT)3 receptor antagonist with 5-HT4 receptor antagonistic activity. This compound, as well as ondansetron and granisetron, dose-dependently inhibited the von Bezold-Jarish reflex, a 5-HT3 receptor-mediated response, after intravenous (i.v.) and intraduodenal (i.d.) dosing to rats. The ID50 values showed FK1052 (0.28 microgram/kg, i.v., 5.23 micrograms/kg, i.d.) to be more potent than ondansetron (5.23 micrograms/kg, i.v., 170 micrograms/kg, i.d.) and granisetron (0.70 micrograms/kg, i.v., 66 micrograms/kg, i.d.). Furthermore, bioavailabilities of the test drugs by ID50 ratio (i.d./i.v.) showed that FK1052(17) was better absorbed than ondansetron(33) and granisetron(94) and possessed a similar duration of action to that of ondansetron and granisetron. We also examined the effects on 2-methyl-5-HT-, 5-HT- and 5-methoxytryptamine-induced contractions of guinea pig isolated ileum. FK1052, ondansetron and granisetron concentration-dependently inhibited 2-methyl-5-HT, a 5-HT3 agonist-induced contraction. The pA2 values for the 5-HT3 receptor indicated that FK1052 (8.36) was 40 times and three times more potent than ondansetron (6.79) and granisetron (7.86), respectively. FK1052, unlike ondansetron and granisetron, inhibited the 5-HT4-mediated component of concentration-response curve to 5-HT. Furthermore, FK1052 suppressed 5-methoxytryptamine, a 5-HT4 agonist-induced contraction in a concentration-dependent but insurmountable manner. (ABSTRACT TRUNCATED AT 250 WORDS)
The AppA and PpsR Proteins from Rhodobacter sphaeroides Can Establish a Redox-Dependent Signal Chain but Fail To Transmit Blue-Light Signals in Other Bacteria

ABSTRACT The AppA protein of Rhodobacter sphaeroides has the unique ability to sense and transmit redox and light signals. In response to decreasing oxygen tension, AppA antagonizes the transcriptional regulator PpsR, which represses the expression of photosynthesis genes, including the puc operon. This mechanism, which is based on direct protein-protein interaction, is prevented by blue-light absorption of the BLUF domain located in the N-terminal part of AppA. In order to test whether AppA and PpsR are sufficient to transmit redox and light signals, we expressed these proteins in three different bacterial species and monitored oxygen- and blue-light-dependent puc expression either directly or by using a luciferase-based reporter construct. The AppA/PpsR system could mediate redox-dependent gene expression in the alphaproteobacteria Rhodobacter capsulatus and Paracoccus denitrificans but not in the gammaproteobacterium Escherichia coli. Analysis of a prrA mutant strain of R. sphaeroides strongly suggests that light-dependent gene expression requires a balanced interplay of the AppA/PpsR system with the PrrA response regulator. Therefore, the AppA/PpsR system was unable to establish light signaling in other bacteria. Based on our data, we present a model for the interdependence of AppA/PpsR signaling and the PrrA transcriptional activator.