Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of ruthenium red on rat heart subcellular calcium transport.

Ruthenium red inhibited Ca2+-ATPase and ATP-independent Ca2+ binding with rat heart sarcolemma in a concentration dependent manner; significant effects were evident at 0.25 microM and higher concentrations. The apparent Ka for Ca2+-ATPase was 1.02 +/- 0.02 mM Ca2+ and 1.47 +/- 0.12 mM Ca2+ in the absence and presence of 2.5 microM ruthenium red, respectively; however, no change in the Vmax (41.2 +/- 1.6 mumol Pi/mg/h) was observed. Likewise, the affinity of Ca2+ for both low and high affinity Ca2+ binding sites in sarcolemma was decreased by ruthenium red. Sarcolemmal Na+-dependent Ca2+ uptake, ATP-dependent Ca2+ accumulation, Mg2+-ATPase and Na+,K+-ATPase activities were not affected by ruthenium red. In sarcoplasmic reticulum preparations, ruthenium red (0.25 to 25 microM) enhanced Ca2+ uptake without altering the Ca2+-stimulated ATPase activity. The observed increase in Ca2+ uptake appears to be due to the depressant effect of the dye on Ca2+ release from the sarcoplasmic reticulum. In mitochondrial preparations, ruthenium red (0.025 to 25 microM) showed a marked inhibitory effect on Ca2+ uptake activity whereas the Mg2+-ATPase activity was unaltered. In isolated rat hearts, 0.025 microM ruthenium red produced a slight negative inotropic effect, whereas 0.25 to 2.5 microM ruthenium red elicited a biphasic response both in terms of developed tension and resting tension. High concentrations of ruthenium red (12.5 to 25 microM) resulted in the development of contracture. Electron microscopic studies revealed the presence of ruthenium red in the myoplasm of hearts perfused for 15 to 30 mins with 2.5 to 5 microM dye. (ABSTRACT TRUNCATED AT 250 WORDS)
Parathyroid Hormone (PTH)-(1–14) and -(1–11) Analogs Conformationally Constrained by α-Aminoisobutyric Acid Mediate Full Agonist Responses via the Juxtamembrane Region of the PTH-1 Receptor*

The N-terminal portion of parathyroid hormone is critical for PTH-1 receptor (P1R) activation and has been postulated to be α-helical when bound to the receptor. We investigated whether substitution of the sterically hindered and helix-promoting amino acid α-aminoisobutyric acid (Aib) in N-terminal PTH oligopeptides would improve the capacity of the peptide to activate the P1R. Analysis of the effects of individual Aib substitutions at each position in [Ala3,12,Gln10,Har11,Trp14]PTH(1–14)NH2([M]PTH(1–14)) on cAMP-stimulating potency in HKRK-B28 cells revealed that Aib at most positions diminished potency; however, Aib at positions 1 and 3 enhanced potency. Thus [Aib1,3,M]PTH(1–14) was ∼100-fold more potent than [M]PTH(1–14) (EC50 = 1.1 ± 0.1 and 100 ± 20 nm, respectively), ∼100,000-fold more potent than native PTH(1–14), and 2-fold more potent than PTH(1–34). The shorter peptide, [Aib1,3,M]PTH(1–11), was also fully efficacious and 1,000-fold more potent than [M]PTH(1–11) (EC504 ± 1 nm versus 3 ± 1 μm). In cAMP stimulation assays performed in COS-7 cells expressing P1R-delNt, a receptor that lacks most of the N-terminal extracellular domain, [Aib1,3,M]PTH(1–14) was 50-fold more potent than [M]PTH(1–14) (EC50 = 0.7 ± 0.2 versus 40 ± 2 nm) and 1,000-fold more potent than PTH(1–34) (EC50 = 700 nm). [Aib1,3,M]PTH(1–14), but not PTH(1–34), inhibited the binding of125I-[Aib1,3,Nle8,Gln10,Har11,Ala12,Trp14,Arg19,Tyr21]PTH(1–21)NH2to hP1R-delNt (IC50 = 1,600 ± 200 nm). The Aib1,3 substitutions in otherwise unmodified PTH(1–34) enhanced potency and binding affinity on hP1R-delNt, but they had no effect for this peptide on hP1R-WT. Circular dichroism spectroscopy demonstrated that the Aib-1,3 substitutions increased helicity in all peptides tested, including PTH(1–34). The overall data thus suggest that the N-terminal residues of PTH are intrinsically disordered but become conformationally constrained, possibly as an α-helix, upon interaction with the activation domain of the PTH-1 receptor.
Mus81 and converging forks limit the mutagenicity of replication fork breakage

How to repair broken replication forks Double-strand breaks in DNA are extremely dangerous to the integrity of our genomes. Most arise from problems encountered by replication forks during duplication of genomic DNA. Break-induced replication is known to use an error-prone DNA polymerase to repair such damage. Mayle et al. show that cells limit error-prone DNA synthesis by preventing the DNA polymerase from inadvertently switching to a related sequence with an incorrect template. The repair of the break is achieved by using a structure-specific nuclease to prevent formation of a long single-stranded region. Science, this issue p. 742 A nuclease prevents DNA polymerase from swinging to the wrong template while repairing broken DNA. Most spontaneous DNA double-strand breaks (DSBs) result from replication-fork breakage. Break-induced replication (BIR), a genome rearrangement–prone repair mechanism that requires the Pol32/POLD3 subunit of eukaryotic DNA Polδ, was proposed to repair broken forks, but how genome destabilization is avoided was unknown. We show that broken fork repair initially uses error-prone Pol32-dependent synthesis, but that mutagenic synthesis is limited to within a few kilobases from the break by Mus81 endonuclease and a converging fork. Mus81 suppresses template switches between both homologous sequences and diverged human Alu repetitive elements, highlighting its importance for stability of highly repetitive genomes. We propose that lack of a timely converging fork or Mus81 may propel genome instability observed in cancer.
A self-recovery technique for highly-available stream processing over local area networks

We present a replication-based and self-recovery-based approach, replica backup, that realizes both continuous and highly-available data stream processing over local area networks. In our approach, we use process-pairs mechanism in which peer operators run in parallel and independently so that each downstream operator can use whichever data arrives first. To further realize continuously stable communication among operators and improve the robustness of system, we devise automatical recovery mechanism that overcomes the limitation of one-off recovery mechanism. In this paper, we first outline the basic design and framework associating with our self-recovery technique. Next, we develop central leader election algorithm (CLEA) that can choose a new operator according with the placement of candidates. This operator placement algorithm that directly measures the latency among operators aims to balance the cost of data stream processing and latency guarantee. Finally, we compare our replica backup method with previous high-available technique through experiments on network simulator ns-3 to demonstrate the utility of our work.
ZigBee and wifi network interface on Wireless Sensor Networks

Wireless Sensor Network using many wireless communication protocols, such as Bluetooth, ZigBee, ultra wideband, and wifi. Wifi has the advantages of high data rate and long range distances, but it requires a great power. While ZigBee has the advantages that it uses less power, but the resulting low data rate and short range distances. With respective these advantages and disadvantages, this paper make interface between ZigBee and wifi communication standards. Data is transmitted by the ZigBee Transceiver then its received and processed by ZigBee and wifi interface. The result of data conversion then transmitted wirelessly to the wifi transceiver, and it will be displayed on a computer. Wifi transceiver has a dual function, receive data and also send the data back to the ZigBee transceiver to display on LCD through the interface. ZigBee and wifi interface is working to convert the data from TCP/IP protocol into ZigBee protocol and applies vice versa. The system can communicate properly when the baud rate is 9600bps.
Modification of the methacholine inhalation test and its epidemiologic use in polyurethane workers.

The dosimeter method of administering doubling cumulative doses of methacholine to measure bronchial responsiveness was standardized to control for the effects of a number of potential influencing variables. The aerodynamic mass median diameter of the challenge aerosol produced from a DeVilbiss 646 nebulizer proved to be 1.2 mu, and the mean output per inhalation 8.9 microliters. Each challenge dose comprised 5 inhalations. Cumulative doses ranged from 0.3 methacholine inhalation units (1 unit = 1 inhalation of aerosol from a 1-mg/ml solution of methacholine, i.e., 8.9 micrograms methacholine) to a possible 640 units, the maximum that was considered reasonable to avoid the risk of unacceptable systemic effects. Responsiveness was expressed as the dose provoking a 20% decline (PD20) in FEV1. Modifications in this full protocol were introduced to facilitate epidemiologic investigations. Physician assessments coupled with baseline measurements of ventilatory function allowed starting at higher dosages for persons with low probability of hyperresponsiveness, thereby shortening the time required for testing to an average of 38 min. In a validation study of 20 persons using both the full and modified protocols, no significant differences were detected between measured PD20 values (geometric means Full versus Modified, 14.83 versus 14.88; r = 0.99). The modified protocol was used to measure bronchial responsiveness in 254 workers exposed to toluene diisocyanate. It proved to be safe and acceptable. Sixty-four workers (25.2%) were found to be reactors. The frequency distribution of the PD20 values exhibited a steadily increasing trend, consistent with a unimodal distribution.
Root Cell-Specific Regulators of Phosphate-Dependent Growth1[OPEN]

In silico analysis of iterative coexpression and protein interaction identifies root cell-enriched regulators of the phosphate starvation response in Arabidopsis with impact on phosphate status, transcriptome, and growth. Cellular specialization in abiotic stress responses is an important regulatory feature driving plant acclimation. Our in silico approach of iterative coexpression, interaction, and enrichment analyses predicted root cell-specific regulators of phosphate starvation response networks in Arabidopsis (Arabidopsis thaliana). This included three uncharacterized genes termed Phosphate starvation-induced gene interacting Root Cell Enriched (PRCE1, PRCE2, and PRCE3). Root cell-specific enrichment of 12 candidates was confirmed in promoter-GFP lines. T-DNA insertion lines of 11 genes showed changes in phosphate status and growth responses to phosphate availability compared with the wild type. Some mutants (cbl1, cipk2, prce3, and wdd1) displayed strong biomass gain irrespective of phosphate supply, while others (cipk14, mfs1, prce1, prce2, and s6k2) were able to sustain growth under low phosphate supply better than the wild type. Notably, root or shoot phosphate accumulation did not strictly correlate with organ growth. Mutant response patterns markedly differed from those of master regulators of phosphate homeostasis, PHOSPHATE STARVATION RESPONSE1 (PHR1) and PHOSPHATE2 (PHO2), demonstrating that negative growth responses in the latter can be overcome when cell-specific regulators are targeted. RNA sequencing analysis highlighted the transcriptomic plasticity in these mutants and revealed PHR1-dependent and -independent regulatory circuits with gene coexpression profiles that were highly correlated to the quantified physiological traits. The results demonstrate how in silico prediction of cell-specific, stress-responsive genes uncovers key regulators and how their manipulation can have positive impacts on plant growth under abiotic stress.
Anoxia-induced extracellular ionic changes in CNS white matter: the role of glial cells.

The rapid changes in brain extracellular ion concentrations that occur with anoxia are important in understanding the pathophysiology of anoxic-ischemic brain injury. While previous studies have focused on the ionic changes that occur in gray matter areas of the brain, white matter (WM) is also damaged by anoxia. We describe the changes in extracellular K+ concentration ([K+]o) and extracellular pH (pHo) that accompany anoxia in WM, and present new results indicating that glial cells directly contribute to the observed fluctuations of these ions. Anoxia-induced changes in [K+]o and pHo were measured with ion-selective microelectrodes in the isolated rat optic nerve, a typical WM tract. To assess the contribution of glial cells, recordings were also made in optic nerves that contained only glial cells (produced by neonatal enucleation). Anoxia in WM produced less extreme changes in [K+]o and pHo than are known to occur in gray matter; in WM during anoxia, the average maximum [K+]o was 14 +/- 2.9 mM (bath [K+]o = 3 mM) and the average maximum acid shift was 0.31 +/- 0.07 pH unit. These extracellular ionic changes were accompanied by rapid shrinkage of extracellular space volume. The ability of optic nerve axons to conduct action potentials was lost in temporal association with the increase in [K+]o. Increasing bath glucose concentration from 10 to 20 mM resulted in a much larger acid shift during anoxia (0.58 +/- 0.08 pH unit) and a smaller average increase in [K+]o (9.2 +/- 2.6 mM). The increased glucose concentration presumably enhanced anaerobic metabolism, leading to extracellular lactate accumulation and a greater acid shift. (ABSTRACT TRUNCATED AT 250 WORDS)
Prevalence of irritable bowel syndrome in the French population according to the Rome I criteria.

BACKGROUND Irritable bowel syndrome (IBS) is a common functional gastro-intestinal disease. In the absence of specific markers, definition and hence diagnosis depend on clinical presentation. Of the various attempts to set criteria for IBS, the most recent are Rome I and Rome II classifications. AIMS To estimate in a general population the prevalence of IBS using the modified Rome I criteria, and to investigate socio-demographic criteria, symptoms and management. METHODS A total of 11,131 people aged 18 years and over, representative of the French population, were surveyed. A diagnostic questionnaire based on the modified Rome I criteria was used to identify IBS sufferers, who were then questioned further about the symptoms and medical management of their IBS. RESULTS Of the 5,299 men and 5,832 women interviewed, 445 had IBS according to the Rome I criteria, a prevalence of 4% (95% CI: 3.6%-4.4%). IBS was more frequent in women (5.3%) than in men (2.5%), with a sex ratio (F/M) of 2.3. In 9.1% of sufferers, onset had occurred less than 12 months ago, a yearly incidence of 3.6 per 1,000 of the population. In 32.3% of IBS sufferers diarrhoea was predominant, and in 34.6% constipation was predominant. Of IBS sufferers 83.7% had consulted a physician for their condition, and 87.6% had taken medication for their IBS symptoms over the previous 12 months. CONCLUSION The prevalence of IBS observed in this study in France was close to the lower limit in published data (3 to 20%). Our results suggest that the Rome I criteria are not sensitive enough to detect all IBS patients in a population not actively seeking health care intervention for the condition. In this regard, the refined classification (Rome II) which was established after our study was carried-out should be evaluated.
ANÁLISIS DEL NIVEL DE RIQUEZA Y DESARROLLO SOCIAL EN LAS REGIONES EUROPEAS

En este trabajo se analizan las regiones europeas en función de su clasificación en términos de riqueza material y la derivada de diversos índices sintéticos de desarrollo utilizando los atributos y variables que lo caracterizan. Con esta finalidad recurrimos en primer lugar a dos indicadores diferentes: uno que sigue la metodología PNUD y otro que aplica el análisis multivariante factorial. Los resultados obtenidos permiten identificar qué regiones transforman mejor el crecimiento en desarrollo social, y qué dimensiones o variables del desarrollo son las responsables de los cambios de posición en los diversos rankings.
The Relationship of Ambient Ozone and PM2.5 Levels and Asthma Emergency Department Visits: Possible Influence of Gender and Ethnicity

ABSTRACT An investigation of the relationship of air pollution and emergency department (ED) visits for asthma was an opportunity to assess environmental risks for asthma exacerbations in an urban population. A total of 6,979 individuals with a primary discharge diagnosis of asthma presented to 1 of 6 EDs in the Pittsburgh, Pennsylvania, area between 2002 and 2005. Using a case-crossover methodology, which controls for the effects of subject-specific covariates such as gender and race, a 2.5% increase was observed in asthma ED visits for each 10 ppb increase in the 1-hour maximum ozone level on day 2 (odds ratio [OR] = 1.025, p < .05). Particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5) had an effect both on the total population on day 1 after exposure (1.036, p < .05), and on African Americans on days 1, 2, and 3. PM2.5 had no significant effect on Caucasian Americans alone. The disparity in risk estimates by race may reflect differences in residential characteristics, exposure to ambient air pollution, or a differential effect of pollution by race.
STAT3 as a Downstream Mediator of Trk Signaling and Functions*

Signal transducer and activator of transcription 3 (STAT3) has long been shown to regulate gene transcription in response to cytokines and growth factors. Recent evidence suggests that STAT3 activation may also occur downstream of receptor-tyrosine kinase activation. In the current study we have identified STAT3 as a novel signal transducer for TrkA, the receptor-tyrosine kinase that mediates the functions of nerve growth factor (NGF). Activation of TrkA by NGF triggered STAT3 phosphorylation at Ser-727, and enhanced the DNA binding and transcriptional activities of STAT3. More importantly, neurotrophin-induced increase in STAT3 activation was observed to underlie several downstream functions of neurotrophin signaling. First of all, knockdown of STAT3 expression using the RNA interference approach attenuated NGF-induced transcription of immediate early genes in PC12 cells. Furthermore, reduced STAT3 expression in PC12 cells suppressed NGF-induced cyclin D1 expression, thereby inhibiting growth arrest normally triggered by NGF treatment. Finally, inhibition of STAT3 expression decreased brain-derived neurotrophic factor-promoted neurite outgrowth in primary hippocampal neurons. Together, our findings have identified STAT3 as an essential component of neurotrophin signaling and functions.
DNA vaccine encoding ESAT‐6 enhances the protective efficacy of BCG against Mycobacterium tuberculosis infection in mice

ESAT‐6 is a protein produced by virulent Mycobacterium tuberculosis but absent in Mycobacterium bovis bacillus Calmette–Guerin (BCG) and is considered as a promising vaccine subunit against tuberculosis. The protective efficacy of a new strategy based on the combination of DNA vaccine encoding ESAT‐6 (DNA‐E6) and BCG immunization was investigated in the present study. BALB/c mice were immunized with DNA‐E6, BCG, DNA‐E6 plus BCG, vector plus BCG or vector alone. Three weeks after the last immunization, antigen‐specific interferon (IFN)‐γ secreted upon stimulation with BCG‐PPD or ESAT‐6 protein by splenocytes of the different groups was determined by an ELISA. The immunized mice were challenged intravenously with low‐dose virulent M. tuberculosis H37Rv and bacterial load of the infected mice was measured in the spleen and lung 6 weeks later. Pathological changes in the lung were observed by haematoxylin–eosin (HE) or acid‐fast staining. Our study demonstrated that ESAT‐6‐specific IFN‐γ was improved in mice vaccinated with DNA‐E6 plus BCG, compared with those mice immunized with BCG alone. The combination of DNA‐E6 and BCG resulted in the maximum reduction in bacterial load in both the lung and spleen, and only slight pathological changes were detected in the lung. These results suggested that the combination of DNA‐E6 and BCG vaccination could be a better strategy against M. tuberculosis infections in human.
Photocatalytic Degradation of NOM for Power Plant Feedwater using Coating and Suspension of TiO2

This study investigated the effectiveness of coating and suspension of Degussa P25 TiO2 photocatalyst to remove natural organic matter (NOM) from surface water for use as power plant feedwater. The catalyst yield, transmittance intensity and X‐ray pattern as a function of the number of coatings were characterized. In addition, P25 coating photocatalytic activity was studied. The photocatalytic activity also of P25 suspension with different catalyst concentrations and the reusing of the catalyst without and with regeneration was investigated. Results obtained show that the P25 coatings were transparent with good adhesion to the glass substrate. P25 suspension was found to be more effective in the NOM photodegradation and gave a higher rate constant compared to P25 coating. The maximum rate constants were 0.028 and 0.015 min−1 at 0.7 g/L P25 suspension and 4 coatings, respectively. After four runs without regeneration and three runs with regeneration of P25 reusing, the photoactivity to remove NOM was still significant.
Implication of the hypoxia response element of the vegf promoter in mouse models of retinal and choroidal neovascularization, but not retinal vascular development

Retinal neovascularization (NV) and macular edema, resulting from blood‐retinal barrier (BRB) breakdown, are major causes of visual loss in ischemic retinopathies. Choroidal NV (CNV) occurs in diseases of the retinal pigmented epithelium/Bruch's membrane complex and is another extremely prevalent cause of visual loss. We used mice in which the hypoxia response element (HRE) is deleted from the vascular endothelial growth factor (vegf) promoter (Vegfδ/δ mice) to explore the role of induction of VEGF through the HRE in these disease processes. Compared to wild type (Vegf+/+) mice with oxygen‐induced ischemic retinopathy (OIR) in which vegf mRNA levels were increased and prominent retinal NV and BRB breakdown occurred, Vegfδ/δ littermates with OIR failed to increase vegf mRNA levels in the retina and had significantly less retinal NV and BRB breakdown, but showed prominent dilation of some superficial retinal vessels. Vegf+/δ littermates with ischemic retinopathy developed comparable retinal NV to Vegf+/+ mice, exhibited intermediate levels of BRB breakdown, and did not show vasodilation. In a mouse model of CNV, due to laser‐induced rupture of Bruch's membrane, the area of CNV at Bruch's membrane rupture sites was more than tenfold greater in Vegf+/+ mice than in Vegfδ/δ littermates. In contrast to these dramatic differences in pathologic ocular NV, Vegfδ/δ mice showed subtle differences in retinal vascular development compared to Vegf+/+ mice; it was slightly delayed, but otherwise normal. These data suggest that induction of VEGF through the HRE in its promoter is critical for retinal and CNV, but not for retinal vascular development. J.Cell. Physiol. © 2005 Wiley‐Liss, Inc.