165 research outputs found

    Transient Raman spectroscopy of 15N-substituted bacteriochlorophyll a. An empirical assignment of T1 Raman lines

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    15N-substituted bacteriochlorophyll a (BChl a) was extracted from the cells of Rhodobacter sphaeroides 2.4.1 grown in a medium containing 15N-ammonium sulfate and yeast concentrate. The T1 Raman spectra of 14N-and 15N-BChl a were obtained as the difference spectra of high-power minus low-power of one-color, pump-and-probe measurements using 420 nm, 5 ns pulses. A set of empirical assignments of the T1 Raman lines was made, based on shifts upon 14N→15N substitution. The S0 Raman spectra of the two BChls were also obtained by using the 457.9 nm cw beam, and a set of assignments of the S0 Raman lines was given for comparison

    Corticosterone Induces Rapid Spinogenesis via Synaptic Glucocorticoid Receptors and Kinase Networks in Hippocampus

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    BACKGROUND: Modulation of dendritic spines under acute stress is attracting much attention. Exposure to acute stress induces corticosterone (CORT) secretion from the adrenal cortex, resulting in rapid increase of CORT levels in plasma and the hippocampus. METHODOLOGY/PRINCIPAL FINDINGS: Here we demonstrated the mechanisms of rapid effect (∼1 h) of CORT on the density and morphology of spines by imaging neurons in adult male rat hippocampal slices. The application of CORT at 100-1000 nM induced a rapid increase in the density of spines of CA1 pyramidal neurons. The density of small-head spines (0.2-0.4 µm) was increased even at low CORT levels (100-200 nM). The density of middle-head spines (0.4-0.5 µm) was increased at high CORT levels between 400-1000 nM. The density of large-head spines (0.5-1.0 µm) was increased only at 1000 nM CORT. Co-administration of RU486, an antagonist of glucocorticoid receptor (GR), abolished the effect of CORT. Blocking a single kinase, such as MAPK, PKA, PKC or PI3K, suppressed CORT-induced enhancement of spinogenesis. Blocking NMDA receptors suppressed the CORT effect. CONCLUSIONS/SIGNIFICANCE: These results imply that stress levels of CORT (100-1000 nM) drive the spinogenesis via synaptic GR and multiple kinase pathways

    Duration of Electrically Induced Atrial Fibrillation Is Augmented by High Voltage of Stimulus with Higher Blood Pressure in Hypertensive Rats

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    Objective. Many previous clinical studies have suggested that atrial fibrillation (AF) is closely associated with hypertension. However, the benefits of antihypertensive therapy on AF are still inconsistent, and it is necessary to explore the factors augmenting AF in hypertensive rats. The aim of the present study was to investigate the correlation between arterial pressure or voltage stimulus and to the duration of electrically induced AF in normotensive or hypertensive rats. Methods. AF was reproducibly induced by transesophageal atrial burst pacing in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We did the burst pacing at high (20 V) or low (5 V) voltage. Results. Duration of AF did not correlate with systolic blood pressure (SBP) and stimulus voltage in WKY. However, only in SHR, duration of AF with high stimulus voltage significantly correlated with SBP and was significantly longer in high than in low voltage stimulus. Discussion and Conclusion. Duration of AF is augmented by high voltage stimulus with higher blood pressure in SHR

    Myelodysplastic syndrome accompanied by basophilia and eosinophilia with t(5;12)(q31;p13)

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    The t(5;12)(q31not, vert, similar35;p12not, vert, similar13) is rare among cytogenetically categorized myeloid diseases. Here we describe a case of myelodysplastic syndrome (MDS) with basophilia followed by leukocytosis, basophilia, and eosinophilia with t(5;12)(q31;p13).A 44-year-old man was referred to Tsukuba University Hospital in August 2005, due to severe anemia and thrombocytopenia. Peripheral blood examination showed hemoglobin 4.5 g/dL, with mean corpuscular volume 109 fL, platelets 73 × 109/L, and white blood cells 4.9 × 109/L with 23% basophils, 3% eosinophils, and 0% blasts. Bone marrow was slightly hypocellular, with trilineage dysplasia. Cytogenetic examination of the bone marrow cells revealed a normal karyotype, 46,XY. A diagnosis of myelodysplastic syndrome–refractory anemia with excess blasts type 2 (MDS-RAEB2) was made according to the WHO classification

    Endogenous Synthesis of Corticosteroids in the Hippocampus

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    BACKGROUND: Brain synthesis of steroids including sex-steroids is attracting much attention. The endogenous synthesis of corticosteroids in the hippocampus, however, has been doubted because of the inability to detect deoxycorticosterone (DOC) synthase, cytochrome P450(c21). METHODOLOGY/PRINCIPAL FINDINGS: The expression of P450(c21) was demonstrated using mRNA analysis and immmunogold electron microscopic analysis in the adult male rat hippocampus. DOC production from progesterone (PROG) was demonstrated by metabolism analysis of (3)H-steroids. All the enzymes required for corticosteroid synthesis including P450(c21), P450(2D4), P450(11β1) and 3β-hydroxysteroid dehydrogenase (3β-HSD) were localized in the hippocampal principal neurons as shown via in situ hybridization and immunoelectron microscopic analysis. Accurate corticosteroid concentrations in rat hippocampus were determined by liquid chromatography-tandem mass spectrometry. In adrenalectomized rats, net hippocampus-synthesized corticosterone (CORT) and DOC were determined to 6.9 and 5.8 nM, respectively. Enhanced spinogenesis was observed in the hippocampus following application of low nanomolar (10 nM) doses of CORT for 1 h. CONCLUSIONS/SIGNIFICANCE: These results imply the complete pathway of corticosteroid synthesis of 'pregnenolone →PROG→DOC→CORT' in the hippocampal neurons. Both P450(c21) and P450(2D4) can catalyze conversion of PROG to DOC. The low nanomolar level of CORT synthesized in hippocampal neurons may play a role in modulation of synaptic plasticity, in contrast to the stress effects by micromolar CORT from adrenal glands

    Synthesis of a Novel Pyrazine-Pyridone Biheteroaryl-Based Fluorescence Sensor and Detection of Endogenous Labile Zinc Ions in Lung Cancer Cells

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    A small extent of endogenous labile zinc is involved in many vital physiological roles in living systems. However, its detailed functions have not been fully elucidated. In this study, we developed a novel biheteroaryl-based low molecular weight fluorescent sensor, 3-(phenylsulfonyl)-pyrazine-pyridone (5b), and applied it for the detection of endogenous labile zinc ions from lung cancer cells during apoptosis. The electron-withdrawing property of the sulfonyl group between the phenyl ring as an electron donor and the pyridone ring as a fluorophore inhibited the intramolecular charge transfer state, and the background fluorescence of the sensor was decreased in aqueous media. From the structure-fluorescence relationship analysis of the substituent effects with/without Zn 2+ , compound 5b acting as a sensor possessed favorable properties, including a longer emission wavelength, a large Stokes shift (over 100 nm),a large fluorescence enhancement in response to Zn 2+ under physical conditions, and good cell membrane permeability in living cells. Fluorescence imaging studies of human lung adenocarcinoma cells (A549) undergoing apoptosis revealed that compound 5b could detect endogenous labile zinc ions. These experiments suggested that the low molecular weight compound 5b is a potential fluorescence sensor for Zn 2+ toward understanding its functions in living systems

    GEOTAIL observation of the SGR1806-20 Giant Flare: The first 600 ms

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    On December 27, 2004, plasma particle detectors on the GEOTAIL spacecraft detected an extremely strong signal of hard X-ray photons from the giant flare of SGR1806-20, a magnetar candidate. While practically all gamma-ray detectors on any satellites were saturated during the first ~500 ms interval after the onset, one of the particle detectors on GEOTAIL was not saturated and provided unique measurements of the hard X-ray intensity and the profile for the first 600 ms interval with 5.48 ms time resolution. After ~50 ms from the initial rapid onset, the peak photon flux (integrated above ~50 keV) reached the order of 10^7 photons sec^{-1} cm^{-2}. Assuming a blackbody spectrum with kT=175 keV, we estimate the peak energy flux to be 21 erg sec^{-1} cm^{-2} and the fluence (for 0-600 ms) to be 2.4 erg cm^{-2}. The implied energy release comparable to the magnetic energy stored in a magnetar (~10^{47} erg) suggests an extremely efficient energy release mechanism.Comment: 6 pages, 2 color figures, submitted to Natur

    Influence of primary and secondary prevention indications on anxiety about the implantable cardioverter-defibrillator

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    AbstractBackgroundImplantable cardioverter-defibrillators (ICDs) have been established for primary and secondary prevention of fatal arrhythmias. However, little is known about the influence of ICD indications on quality of life (QOL) and psychological disturbances. This study aimed to examine whether there were differences in QOL and psychological distress in patients that have an ICD for primary or secondary prevention of fatal arrhythmias.MethodsA multicenter survey of 179 consecutive outpatients (29.1% primary prevention) with ICD implantations completed the Short Form-8 (SF-8), Beck Depression Inventory (BDI), Impact of Event Scale-Revised (IES-R), State-Trait Anxiety Inventory (STAI), and Worries about ICD (WAICD).ResultsPatients with an ICD for primary prevention had a higher trait anxiety score and worries about ICD score than patients with an ICD for secondary prevention (41.7±12.4 vs. 34.7±12.3, p=0.001 and 39.6±18.0 vs. 30.0±18.9, p=0.002, respectively), even after adjusting for demographic and clinical characteristics. In multivariable analysis of variance, primary prevention ICD recipients reported a poorer QOL on the vitality subscale of the SF-8.ConclusionsIn our study population, which mostly consisted of New York Heart Association (NYHA) class I and II subjects, primary prevention ICD recipients were more prone to experience worries about their ICD, anxiety, and a poorer QOL compared to secondary prevention ICD recipients. In clinical practice, primary prevention ICD patients should be closely monitored. If warranted, they should be offered psychological intervention, as anxiety and low QOL were predictors of mortality
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