Miracle-dz/UniFAR-FTUs huggingface dataset:
The influence of TSA and VPA on the in vitro differentiation of bone marrow mesenchymal stem cells into neuronal lineage cells: Gene expression studies.

INTRODUCTION Epigenetic mechanisms regulate the transcription of genes, which can affect the differentiation of MSCs. The aim of the current work is to determine how the histone deacetylase inhibitors TSA and VPA affect the expression of neuronal lineage genes in a culture of rat MSCs (rMSCs). MATERIALS AND METHODS We analyzed the expression of early neuron marker gene (Tubb3), mature neuron markers genes (Vacht, Th, Htr2a) and the oligodendrocyte progenitor marker gene (GalC). Moreover, changes in the gene expression after three different periods of exposure to TSA and VPA were investigated for the first time. RESULTS After six days of exposition to TSA and VPA, the expression of Tubb3 and GalC decreased, while the expression of Th increased. The highest increase of VAChT expression was observed after three days of TSA and VPA treatment. A decrease in Htr2a gene expression was observed after TSA treatment and an increase was observed after VPA treatment. We also observed that TSA and VPA inhibited cell proliferation and the formation of neurospheres in the rMSCs culture. DISCUSSION The central findings of our study are that TSA and VPA affect the expression of neuronal lineage genes in an rMSCs culture. After exposure to TSA or VPA, the expression of early neuronal gene decreases but equally the expression of mature neuron genes increases. After TSA and VPA treatment ER of the oligodendrocyte progenitor marker decreased. TSA and VPA inhibit cell proliferation and the formation of neurospheres in rMSCs culture.
Planning, scheduling, and control for automatic telescopes

This paper presents an argument for the appropriateness of Entropy Reduction Engine (ERE) technology to the planning, scheduling, and control components of Automatic Photoelectric Telescope (APT) management. The paper is organized as follows. In the next section, we give a brief summary of the planning and scheduling requirements for APTs. Following this, in section 3, we give an ERE project precis, couched primarily in terms of project objectives. Section 4 gives a sketch of the match-up between problem and technology, and section 5 outlines where we want to go with this work.
Endothelial cells interact with the core protein of basement membrane perlecan through beta 1 and beta 3 integrins: an adhesion modulated by glycosaminoglycan

Aortic endothelial cells adhere to the core protein of murine perlecan, a heparan sulfate proteoglycan present in endothelial basement membrane. We found that cell adhesion was partially inhibited by beta 1 integrin-specific mAb and almost completely blocked by a mixture of beta 1 and alpha v beta 3 antibodies. Furthermore, adhesion was partially inhibited by a synthetic peptide containing the perlecan domain III sequence LPASFRGDKVTSY (c-RGD) as well as by GRGDSP, but not by GRGESP. Both antibodies contributed to the inhibition of cell adhesion to immobilized c-RGD whereas only beta 1-specific antibody blocked residual cell adhesion to proteoglycan core in the presence of maximally inhibiting concentrations of soluble RGD peptide. A fraction of endothelial surface-labeled detergent lysate bound to a core affinity column and 147-, 116-, and 85-kD proteins were eluted with NaCl and EDTA. Polyclonal anti-beta 1 and anti-beta 3 integrin antibodies immunoprecipitated 116/147 and 85/147 kD surface-labeled complexes, respectively. Cell adhesion to perlecan was low compared to perlecan core, and cell adhesion to core, but not to immobilized c-RGD, was selectively inhibited by soluble heparin and heparan sulfates. This inhibition by heparin was also observed with laminin and fibronectin and, in the case of perlecan, was found to be independent of heparin binding to substrate. These data support the hypothesis that endothelial cells interact with the core protein of perlecan through beta 1 and beta 3 integrins, that this binding is partially RGD- independent, and that this interaction is selectively sensitive to a cell-mediated effect of heparin/heparan sulfates which may act as regulatory ligands.
Enhanced Type 1 Immunity After Secondary Viral Challenge in Mice Primed as Neonates1

The goal of infant immunization against viral infection is to develop protective long term memory responses. Priming neonatal mice with a low dose of Cas-Br-E murine leukemia virus (Cas) results in adult-like, type 1 protective responses. However, other studies suggest that Ag priming of neonates leads to an increase in type 2 secondary responses even when primary responses were type 1. We assessed whether type 1 CD8+ T cell-mediated responses developed in murine neonates are maintained after secondary challenge with Cas in adulthood. Despite the induction of significant anti-viral CD8+-mediated cytotoxic T lymphocyte and IFN-γ responses, initial neonatal priming led to a lower frequency of virus-specific T cells compared with adult priming. Adult frequencies were reached in mice primed as neonates only after secondary challenge in adulthood. A nonspecific and transient CD4+-mediated IL-4 response was present in all groups after secondary challenge with Cas or medium, indicating that this rise in type 2 cytokine production was not unique to mice that had been primed as neonates. Rather, type 1 anti-viral memory CD8+ T cell responses developed in neonatal mice are stable, protective, and enhanced after secondary challenge.
Nitric oxide induces rapid, calcium‐dependent release of vesicular glutamate and ATP from cultured rat astrocytes

Nitric oxide (NO; 1 μM) or an NO donor (500 μM diethylenetriamine‐nitric oxide, DETA‐NONOate) caused rapid glutamate and ATP release from cultured rat cortical astrocytes. NO‐induced glutamate release was prevented by calcium chelators (EGTA or BAPTA‐AM) and an inhibitor of vesicular exocytosis (botulinum neurotoxin C, BoTx‐C), but not by a glutamate transport inhibitor, L‐trans‐pyrrolidine‐2,4‐dicarboxylate (t‐PDC), a cyclooxygenase inhibitor (indomethacin), or an inhibitor of soluble guanylate cyclase 1H‐[1,2,4]oxadiazolo‐[4,3‐a]quinoxalin‐1‐one (ODQ), and was not induced by mitochondrial respiratory inhibitors (myxothiazol or azide). Similarly to glutamate, NO‐induced ATP release was also completely blocked by BAPTA‐AM and BoTx‐C, suggesting again a vesicular, calcium‐dependent mechanism of release. Addition of DETA‐NONOate (500 μM) to fura‐2–loaded astrocytes induced a rapid, transient increase in intracellular calcium levels followed by a lower, sustained level of calcium entry. The latter was blocked by gadolinium (1 μM), an inhibitor of capacitative Ca2+ entry. Thus, NO appears to cause rapid exocytosis of vesicular glutamate and ATP from astrocytes by raising intracellular calcium levels. Astrocytes activated by lipopolysaccharide/endotoxin and interferon‐γ to express inducible NO synthase (iNOS) maintained substantially higher extracellular glutamate levels than nonactivated cells or activated cells treated with an iNOS inhibitor (1400W), but the rate of glutamate uptake by these cells was similar. This suggests that NO from inflammatory‐activated astrocytes causes release of astrocytic glutamate. NO‐induced release of astrocytic glutamate and ATP may be important in physiological or pathological communication between astrocytes and neurons. GLIA 40:312–323, 2002. © 2002 Wiley‐Liss, Inc.
Dispensed selective and nonselective nonsteroidal anti-inflammatory drugs and the risk of moderate to severe hyperkalemia: a nested case-control study.

BACKGROUND It is not known whether nonselective and cyclooxygenase 2 (COX-2) selective nonsteroidal anti-inflammatory drugs (NSAIDs) differ in terms of hyperkalemia risk. The aim of this study was to compare the differential risk of hyperkalemia associated with various NSAIDs. STUDY DESIGN Nested case-control study. SETTING & PARTICIPANTS New NSAID users receiving care in the US Department of Veterans Affairs (VA) health care system from October 2000 to September 2006. PREDICTOR OF FACTOR: Different NSAIDs ordered by COX-2 selectivity. OUTCOMES & MEASUREMENTS Risk of hyperkalemia (defined as first serum potassium value ≥6.0 mEq/L) was estimated with a multivariate conditional logistic model adjusting for age, race, morbidities, medications, and contrast media. RESULTS We identified 18,326 cases of hyperkalemia and 355,106 matched controls. Risk of hyperkalemia did not differ in patients using a single NSAID (adjusted OR, 1.03; 95% CI, 0.98-1.08) or 2 or more NSAIDs (OR, 1.16; 95% CI, 0.96-1.41) compared with patients no longer using an NSAID. However, risk varied by specific NSAID and elevated risks were found for use of rofecoxib, celecoxib, diclofenac, and indomethacin, but not meloxicam, etodolac, piroxicam, sulindac, ibuprofen, naproxen, and ketorolac. Interactions were found between NSAID use and exposure to renin-angiotensin blockers and contrast media. LIMITATIONS Some NSAIDs are available over the counter and women are under-represented in the VA population. CONCLUSIONS NSAIDs may not by themselves carry a higher risk of moderate to severe hyperkalemia. Certain NSAIDs may increase the risk of hyperkalemia, but it is not related to COX-2 selectivity of the NSAID and may depend on concurrent exposure to other agents.
Vascular Outcome in Patients With Homocystinuria due to Cystathionine &bgr;-Synthase Deficiency Treated Chronically: A Multicenter Observational Study

An inborn error of metabolism, homocystinuria due to cystathionine &bgr;-synthase deficiency, results in markedly elevated levels of circulating homocysteine. Premature vascular events are the main life-threatening complication. Half of all untreated patients have a vascular event by 30 years of age. We performed a multicenter observational study to assess the effectiveness of long-term homocysteine-lowering treatment in reducing vascular risk in 158 patients. Vascular outcomes were analyzed and effectiveness of treatment in reducing vascular risk was evaluated by comparison of actual to predicted number of vascular events, with the use of historical controls from a landmark study of 629 untreated patients with cystathionine &bgr;-synthase deficiency. The 158 patients had a mean (range) age of 29.4 (4.5 to 70) years; 57 (36%) were more than 30 years old, and 10 (6%) were older than 50 years. There were 2822 patient-years of treatment, with an average of 17.9 years per patient. Plasma homocysteine levels were markedly reduced from pretreatment levels but usually remained moderately elevated. There were 17 vascular events in 12 patients at a mean (range) age of 42.5 (18 to 67) years: pulmonary embolism (n=3), myocardial infarction (n=2), deep venous thrombosis (n=5), cerebrovascular accident (n=3), transient ischemic attack (n=1), sagittal sinus thrombosis (n=1), and abdominal aortic aneurysm (n=2). Without treatment, 112 vascular events would have been expected, for a relative risk of 0.09 (95% CI 0.036 to 0.228;P <0.0001). Treatment regimens designed to lower plasma homocysteine significantly reduce cardiovascular risk in cystathionine &bgr;-synthase deficiency despite imperfect biochemical control. These findings may be relevant to the significance of mild hyperhomocysteinemia that is commonly found in patients with vascular disease.
Opportunities for power quality improvement through DG-grid interfacing converters

Power electronics technology is becoming an increasingly important aspect of today's power distribution system. It is the key interface to connect distributed energy resource (DER) to the utility and the local loads. With the increased penetration of power electronics based distributed generation (DG) systems, the power quality requirements are becoming more stringent. On the other hand, if controlled and regulated properly, the DG-grid interfacing converters are able to improve the system efficiency and power quality, in addition to the primary function of real power injection. This paper discusses the opportunities for power quality improvement through the DG-grid interfacing converters. While the harmonic voltage compensation is the focus of this paper, a number of other ancillary functions, such as unbalance voltage compensation, voltage sag mitigation and reactive power compensation, can be realized in a similar manner. Two alternative DG control methods, namely current controlled DG and voltage controlled DG, are considered and the associated power quality compensation strategies are developed. Simulation results and experimental results from a three-phase 5kVA laboratory DG prototype are provided.
A sensitivity analysis of SPICE parameters using an eleven-stage ring oscillator

SPICE is a circuit simulator which predicts node voltages and currents as a function of time from device model parameters. Model parameters are determined by the manufacturing process, but process-induced variations in these parameters occur within a chip or from chip to chip. Values for the model parameters used in simulators are usually obtained from measurements on test structures along the periphery of the circuit or in test chips located at several sites on the product wafer. This paper presents examples of how well model parameters extracted from a test chip can predict the AC response of a dynamic circuit element (MOS ring oscillator) on the same wafer. Simulation results show which model parameters are critical to performance. A comparison between measurement and simulation results is given and the importance of intrachip and intrawafer parameter variations is discussed. For the samples tested, the polysilicon gate linewidth variation was determined to be the primary cause of the ring oscillator frequency variation.
Discussion of “Representation of People’s Decisions in Health Information Systems: A Complementary Approach for Understanding Health Care Systems and Population Health”

Summary This article is part of a For-Discussion-Section of Methods of Information in Medicine about the paper “Representation of People’s Decisions in Health Information Systems: A Complementary Approach for Understanding Health Care Systems and Population Health” written by Fernan Gonzalez Bernaldo de Qui-ros, Adriana Ruth Dawidowski, and Silvana Figar. It is introduced by an editorial. This article contains the combined commentaries invited to independently comment on the paper of de Quiros, Dawidowski, and Figar. In subsequent issues the discussion can continue through letters to the editor.
A Parameterization of Shear-Driven Turbulence for Ocean Climate Models

Abstract This paper presents a new parameterization for shear-driven, stratified, turbulent mixing that is pertinent to climate models, in particular the shear-driven mixing in overflows and the Equatorial Undercurrent. This parameterization satisfies a critical requirement for climate applications by being simple enough to be implemented implicitly and thereby allowing the parameterization to be used with time steps that are long compared to both the time scale on which the turbulence evolves and the time scale with which it alters the large-scale ocean state. The mixing is expressed in terms of a turbulent diffusivity that is dependent on the shear forcing and a length scale that is the minimum of the width of the low Richardson number region (Ri = N 2/|uz|2, where N is the buoyancy frequency and |uz| is the vertical shear) and the buoyancy length scale over which the turbulence decays [Lb = Q1/2/N, where Q is the turbulent kinetic energy (TKE)]. This also allows a decay of turbulence vertically away fr.
Iron-Mediated Control of the Basic Helix-Loop-Helix Protein FER, a Regulator of Iron Uptake in Tomato1

Root iron mobilization genes are induced by iron deficiency downstream of an unknown signaling mechanism. The FER gene, encoding a basic helix-loop-helix domain protein and putative transcription factor, is required for induction of iron mobilization genes in roots of tomato (Lycopersicon esculentum). To study upstream regulatory events of FER action, we examined the control of FER gene and FER protein expression in response to iron nutritional status. We analyzed expression of the FER gene and FER protein in wild-type plants, in mutant plants with defects in iron uptake regulation, and in 35S transgenic plants that overexpressed the FER gene. An affinity-purified antiserum directed against FER epitopes was produced that recognized FER protein in plant protein extracts. We found that the FER gene and FER protein were consistently down-regulated in roots after generous (100 μm, physiologically optimal) iron supply compared to low (0.1 μm) and sufficient (10 μm) iron supply. FER gene and FER protein expression were also occasionally down-regulated at sufficient compared to low iron supply. Analysis of FER protein expression in FER overexpression plants, as well as cellular protein localization studies, indicated that FER was down-regulated by high iron at the posttranscriptional level. The FER protein was targeted to plant nuclei and showed transcriptional activation in yeast (Saccharomyces cerevisiae). FER protein regulation in the iron accumulation mutant chloronerva indicated that FER protein expression was not directly controlled by signals derived from iron transport. We conclude that FER is able to affect transcription in the nucleus and its action is controlled by iron supply at multiple regulatory levels.
Utilization and metabolism of palmityl and oleoyl fatty acids and alcohols in caecal enterocytes of Atlantic salmon (Salmo salar L.)

The substitution of fish oil with wax ester-rich calanoid copepod-derived oil in diets for carnivorous fish, such as Atlantic salmon, has previously indicated lower lipid digestibility. This suggests that the fatty alcohols (FAlc) present in wax esters may be a poorer substrate for intestinal enzymes than the fatty acids (FA) in triacylglycerol (TAG), the major lipid in fish oil. The hypothesis tested was that the possible lower utilization of dietary FAlc by salmon enterocytes is at the level of uptake and that subsequent intracellular metabolism was identical to that of FA. A dual-labelled FAlc–FA metabolism assay was employed to determine simultaneous FAlc and FA uptake and relative utilization in enterocytes isolated from pyloric caeca of Atlantic salmon fed either a diet supplemented with fish oil or wax ester-rich Calanus oil. The diets were fed for 10 weeks before caecal enterocytes from each dietary group were isolated and incubated with equimolar mixtures of either [1-14C]16:0 FA and [9,10(n)-3H]16:0 FAlc, or [1-14C]18:1n-9 FA and [9,10(n)-3H] 18:1n-9 FAlc. Uptake was measured after 2 h with relative utilization of labelled FAlc and FA calculated as a percentage of uptakes. Differences in uptake were observed, with FA showing higher uptake than FAlc, and 18:1 chains a higher uptake than 16:0. A proportion of unesterified FAlc was possibly recovered in the cells, but the majority of FAlc was recovered in lipid classes such as TAG and phospholipids indicating substantial conversion of FAlc to FA followed by esterification. However, incorporation of FA and FAlc into esterified lipids was higher when derived from FA than from FAlc. Twenty-five to fifty percentage of the absorbed 16:0 FA was recovered in TAG fraction of the enterocytes compared with 15–75% of 18:1 FA. Twenty to thirty percentage of the absorbed 16:0 FA was recovered in the phosphatidylcholine fraction of the enterocytes compared with only 5–15% of the 18:1 FA. Less than 15% of the fatty chains taken up by the cells were used for energy production, with significantly higher oxidation of 18:1 in enterocytes from fish fed the fish oil diet compared with the Calanus oil diet. However, overall, dietary copepod oil had little effect on FAlc and FA metabolism. Metabolic modification by elongation and/or desaturation was generally low at 1–5% of the uptake. We conclude that our hypothesis was generally proved in that the uptake of FAlc by salmon enterocytes was lower than the uptake of FA and that subsequent intracellular metabolism of FAlc was similar to that of FA. However, unesterified FAlc was possibly recovered in the cells suggesting that the conversion to FA may not be concomitant with uptake.
Prefrontal Cortex and Working Memory Processes Article in Press

—Working memory is a mechanism for short-term active maintenance of information as well as for processing maintained information. The dorsolateral prefrontal cortex has been known to participate in working memory. The analysis of task-related dorsolateral prefrontal cortex activity while monkeys performed a variety of working memory tasks revealed that delay-period activity is a neural correlate of a mechanism for temporary active maintenance of information, because this activity persisted throughout the delay period, showed selectivity to a particular visual feature, and was related to correct behavioral performances. Information processing can be considered as a change of the information represented by a population of neural activities during the progress of the trial. Using population vectors calculated by a population of task-related dorsolateral prefrontal cortex activities, we demonstrated the temporal change of information represented by a population of dorsolateral prefrontal cortex activities during performances of spatial working memory tasks. Cross-correlation analysis using spike firings of simultaneously isolated pairs of neurons reveals widespread functional interactions among neighboring neurons, especially neurons having delay-period activity, and their dynamic modulation depending on the context of the trial. Functional interactions among neurons and their dynamic modulation could be a mechanism of information processing in the dorsolateral prefrontal cortex. Working memory has been described as a system that provides temporary active maintenance of information and also enables manipulation and processing of information (Baddeley, 1986; Baddeley and Hitch, 1974). Working memory has been thought to participate significantly in higher cognitive functions such as thinking, planning, reasoning , decision-making, and language comprehension. Therefore, it is expected that understanding neural mechanisms of working memory could provide important clues to understand mechanisms of these cognitive functions. Several models of working memory have been proposed (Miyake and Shah 1999). Among these, the most well-known and influential model of working memory is the one proposed by Baddeley and Hitch (1974) and Baddeley (1986, 2000). Baddeley's model of working memory includes one master component (the central executive) and three slave components (the visuospatial sketchpad, the phonological loop, and the episodic buffer). Among slave components, the phonological loop is a system for performing speech perception and language comprehension and includes a mechanism for temporarily maintaining speech-based information by subvocal rehearsal. The visuospatial sketchpad is a system for processing visuo-spatial information as well as information that cannot be expressed by language and includes a mechanism for temporarily maintaining information as visuo-spatial images by a rehearsal system. The episodic …
Polo kinase Cdc5 is a central regulator of meiosis I

During meiosis, two consecutive rounds of chromosome segregation yield four haploid gametes from one diploid cell. The Polo kinase Cdc5 is required for meiotic progression, but how Cdc5 coordinates multiple cell-cycle events during meiosis I is not understood. Here we show that CDC5-dependent phosphorylation of Rec8, a subunit of the cohesin complex that links sister chromatids, is required for efficient cohesin removal from chromosome arms, which is a prerequisite for meiosis I chromosome segregation. CDC5 also establishes conditions for centromeric cohesin removal during meiosis II by promoting the degradation of Spo13, a protein that protects centromeric cohesin during meiosis I. Despite CDC5’s central role in meiosis I, the protein kinase is dispensable during meiosis II and does not even phosphorylate its meiosis I targets during the second meiotic division. We conclude that Cdc5 has evolved into a master regulator of the unique meiosis I chromosome segregation pattern.