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At least 739 records · Page 41Linked to original sources

Measurement of bottom-quark hadron masses in exclusive J/psi decays with the CDF detector.

We measure the masses of b hadrons in exclusively reconstructed final states containing a J/psi --> mu-mu+ decay using 220 pb(-1) of data collected by the CDF II experiment. We find: m(B+) = 5279.10 +/- 0.41(stat.) +/- 0.36(sys.) MeV/c2, m(B0) = 5279.63 +/- 0.53(stat.) +/- 0.33(sys.) MeV/c2, m(B(s)0) = 5366.01 +/- 0.73(stat.) +/- 0.33(sys.) MeV/c2, m(lambda(b)0) = 5619.7 +/- 1.2(stat.) +/- 1.2(sys.) MeV/c2. m(B+) - m(B0) = -0.53 +/- 0.67(stat.) +/- 0.14(sys.) MeV/c2, m(B(s)0) - m(B0) = 86.38 +/- 0.90(stat.) +/- 0.06(sys.) MeV/c2, m(lambda(b)0) - m(B0) = 339.2 +/- 1.4(stat.) +/- 0.1(sys.) MeV/c2. The measurements of the B(s)0, lambda(b)0 mass, m(B(s)0) - m(B0) and m(lambda(b)0) - m(B0) mass difference are of better precision than the current world averages.

Journal Article↗

Differential Accumulation of Sunflower Tetraubiquitin mRNAs during Zygotic Embryogenesis and Developmental Regulation of Their Heat-Shock Response.

We have isolated and sequenced Ha UbiS, a cDNA for a dry-seed-stored mRNA that encodes tetraubiquitin. We have observed differential accumulation of tetraubiquitin mRNAs during sunflower (Helianthus annuus L.) zygotic embryogenesis. These mRNAs were up-regulated during late embryogenesis and reached higher prevalence in the dry seed, where they were found to be associated mainly with provascular tissue. UbiS mRNA, as confirmed by Rnase A protection experiments, accumulated also in response to heat shock, but only in leaves and later during postgerminative development. These novel observations demonstrate expression during seed maturation of specific plant polyubiquitin transcripts and developmental regulation of their heat-shock response. Using ubiquitin antibodies we also detected discrete, seed-specific proteins with distinct temporal expression patterns during zygotic embryogenesis. Some of these patterns were concurrent with UbiS mRNA accumulation in seeds. The most abundant ubiquitin-reacting proteins found in mature seeds were small (16-22 kD) and acidic (isoelectric points of 6.1-7.4). Possible functional implications for UbiS expression elicited from these observations are discussed.

Journal Article↗

A nitrilase-like protein interacts with GCC box DNA-binding proteins involved in ethylene and defense responses.

Ethylene-responsive element-binding proteins (EREBPs) of tobacco (Nicotiana tabacum L.) bind to the GCC box of many pathogenesis-related (PR) gene promoters, including osmotin (PR-5). The two GCC boxes on the osmotin promoter are known to be required, but not sufficient, for maximal ethylene responsiveness. EREBPs participate in the signal transduction pathway leading from exogenous ethylene application and pathogen infection to PR gene induction. In this study EREBP3 was used as bait in a yeast two-hybrid interaction trap with a tobacco cDNA library as prey to isolate signal transduction pathway intermediates that interact with EREBPs. One of the strongest interactors was found to encode a nitrilase-like protein (NLP). Nitrilase is an enzyme involved in auxin biosynthesis. NLP interacted with other EREBP family members, namely tobacco EREBP2 and tomato (Lycopersicon esculentum L.) Pti4/5/6. The EREBP2-EREBP3 interaction with NLP required part of the DNA-binding domain. The specificity of interaction was further confirmed by protein-binding studies in solution. We propose that the EREBP-NLP interaction serves to regulate PR gene expression by sequestration of EREBPs in the cytoplasm.

Amino Acid Sequence↗

Abnormal Na+-K+ ATPase kinetics in a subset of essential hypertensive patients.

We have performed a kinetic analysis of the interaction of Na+-K+ ATPase with internal Na+ in erythrocytes of 30 normotensive controls and 72 essential hypertensive patients. Neither the maximal rate of ouabain-sensitive sodium efflux (Vmax) nor the internal Na+ content required for half-maximal stimulation (K50%) were significantly different between normotensive and hypertensive patients. Nevertheless, using the 95% confidence limits of the K50% in the normotensive group as a cut-off point, 13 (18.06%) essential hypertensive patients exhibited increased values of this parameter (29.16 +/- 4.31 mmol l-1 cells) revealing decreased affinity of Na+-K+ ATPase for internal Na+ (Pump-hypertensives). The Vmax was also higher in the Pump '-' subset (14.08 +/- 4.85 mmol (1 cells h)-1 vs. 6.92 +/- 1.80; P = 0.0002) and 10 of these 13 hypertensives exhibited a Vmax above the upper end limit of 10.5 mmol (1 cells h)-1, suggesting a compensatory effect. No differences were observed between the Pump '-' subset and the remaining 59 hypertensives without Na+-K+ pump abnormality when basal erythrocyte Na+ content and clinical parameters of hypertension were examined. Decreased apparent affinity of Na+-K+ pump for internal Na+ present in 9-27% of essential hypertensives may be implicated in pathogenetic mechanisms of hypertension.

Adult↗

Relationship between apoptosis and proliferation in secondary tumors of the brain.

A correlation between apoptosis and proliferation in astrocytomas and oligodendrogliomas, but not in glioblastomas, has been previously reported. An index for apoptosis and proliferation was established for each tumor in a series of 20 brain metastases, and its correlation was studied using the Spearman rank correlation test. Apoptosis index (AI) ranged between 1 and 78% (mean SD: 11.48+/-16.4). Proliferation index (PI) ranged between 2.4 and 21% (mean+/-SD: 8.23+/-4.8). When the relationship between AI and PI was studied, a clear correlation was found (r: 0.8965, 95% CI: 0.74-0.95; P < 0.0001). Therefore, it is concluded that a clear correlation exists between proliferation and apoptosis in secondary tumors of the brain.

Adult↗

Effect of intravenous iron on haemodialysis catheter microbial colonization and blood-borne infection.

BACKGROUND: Intravenous (i.v.) iron is employed to treat absolute and relative iron deficiency in end-stage renal disease patients. However, there exists the possibility that i.v. iron increases infection risk. This pilot study examines whether i.v. iron gluconate acutely increases tunnelled haemodialysis catheter colonization, microbial growth, or blood-borne infection. METHODS: Nineteen patients with haemodialysis catheters who met criteria to receive an i.v. iron load entered the study. Six matched patients with catheters who did not receive iron were controls. Blood aspirated from the catheter prior to initiation of haemodialysis was sent for qualitative/quantitative cultures. The study consisted of three baseline cultures, five cultures during iron (125 mg of ferric gluconate per treatment), and three cultures following iron administration. Patients were monitored for infection for 30 days following iron. RESULTS: Fifteen iron-treated patients and six controls completed the study. Thirty-three per cent of treated patients were colonized at baseline; 66% were colonized following iron. Thirty-three per cent of controls (2/6) were colonized at baseline; no new colonization developed during follow up. Neither treated patients nor controls had significant microbial growth within catheters; one patient in the iron-treated group developed candidaemia. CONCLUSION: Intravenous iron is not associated with acute microbial growth in catheters or clinical infection. However, a trend towards increased catheter colonization following iron administration exists.

Adult↗

Hyposmotically activated chloride channels in cultured rabbit non-pigmented ciliary epithelial cells.

1. We used whole-cell patch-clamp recording techniques and noise analysis of whole-cell current to investigate the properties of hyposmotic shock (HOS)-activated Cl- channels in SV40-transformed rabbit non-pigmented ciliary epithelial (NPCE) cells. 2. Under conditions designed to isolate Cl- currents, exposure of cells to hyposmotic external solution reversibly increased the whole-cell conductance. 3. The whole-cell current activated with a slow time course (> 15 min), exhibited outward rectification and was Cl- selective. 4. The disulphonic stilbene derivatives 4, 4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 0.5 mM), 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS, 0. 5 mM) and 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS, 0.5 mM) produced a voltage-sensitive block of HOS-activated Cl- current at depolarized potentials, whereas niflumic acid produced a voltage-independent block of the current. 5. Under Ca2+-free conditions, HOS stimulation still reversibly activated the Cl- current, but the amplitude of current was reduced and the time course of current activation was slower compared with control (P < 0. 05). 6. The non-specific kinase inhibitor H-7 (100 microM), upregulated HOS-activated Cl- current amplitude in all cells tested (P < 0.05). 7. Noise analysis of whole-cell Cl- current indicated that cell swelling activated a high density of small conductance Cl- channels (< 1 pS). 8. We conclude that HOS primarily activates a high density of volume-sensitive small conductance Cl- channels in rabbit NPCE cells, and that Ca2+ and phosphorylation are involved in channel regulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Tamoxifen and ATP synergistically activate Cl- release by cultured bovine pigmented ciliary epithelial cells.

Purines alter aqueous humour secretion by the bilayered ciliary epithelium. Adenosine but not ATP shrinks non-pigmented ciliary epithelial (NPE) cells by activating Cl- channels. We now report effects of ATP on pigmented ciliary epithelial (PE) cells. Cultured bovine PE cells were studied volumetrically by electronic cell sorting. ATP and tamoxifen acted synergistically to shrink PE cells. Neither ATP nor tamoxifen alone had a consistent effect on cell volume. The tamoxifen, ATP-activated shrinkage required Cl- release since the response was blocked by removing Cl- and was inhibited by the Cl- channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoate and 4,4'-diisothiocyano-2,2'-disulfonic acid. The modulating effect of tamoxifen could have reflected many actions of tamoxifen. Our data do not support the suggestion that tamoxifen inhibits protein kinase C (PKC) or calcium-calmodulin, or that it acts on histamine or carbachol receptors. The shrinkage produced by ATP and tamoxifen was blocked by 17beta-oestradiol, but not 17alpha-oestradiol. The cooperative interaction between tamoxifen and ATP was not mediated by an enhanced rise in [Ca2+]i. The results indicate that tamoxifen interacts synergistically with ATP to activate Cl- release by the PE cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Relation of left ventricular hypertrophy to regional cerebral blood flow: single photon emission computed tomography abnormalities in essential hypertension.

Several reports have shown that left ventricular hypertrophy (LVH) is an independent predictor of acute cerebrovascular events. The aim of the present study was to investigate the relationship between LVH and cerebral blood flow in middle-aged patients with essential hypertension. Forty never-treated hypertensive patients (24 men, 16 women, aged 50-60 years) without clinical evidence of target organ damage were studied. Regional cerebral blood flow was measured by means of single photon emission computed tomography of the brain. Twenty-nine patients showed echocardiographic criteria of LVH; 11 patients did not show this feature. No differences were found in regional cerebral blood flow ratio of all brain areas studied between hypertensives with or without LVH except for the striatum area. The regional cerebral blood flow ratio was significantly reduced in the striatum region of hypertensive patients with LVH, compared with patients without LVH (91.5+/-7.4 vs 98.1+/-8.3; P=.023). This relationship remained significant after adjusting for blood pressure. The authors conclude that the presence of LVH in middle-aged patients with essential hypertension is associated with a reduction of regional cerebral blood flow in the striatum area.

Blood Pressure↗

Disturbances in Na+ transport systems induced by ethanol in human red blood cells.

The effects of ethanol on fluxes catalyzed by four Na+ transport systems (ouabain-sensitive Na+, K+ pump, bumetanide-sensitive Na+, K+ cotransport system, Na+:Li+- countertransport and anion carrier) and on Na+ and K+ leaks were investigated in human red blood cells. Ethanol concentrations higher than 32 mM were required in order to significantly modify erythrocyte Na+ transport function. The observed changes can be summarized as follows: (a) stimulation of Na+ efflux through the Na+, K+ pump (by 21-32% at 160-400 mM) and Na+:Li+ countertransport (by 34-59% at 160-400 mM); (b) inhibition of outward Na+, K+ cotransport (by 23-34% at 160-400 mM) and LiCO3- influx through the anion carrier (by 17-21% at 64-400 mM); and (c) increase in Na+ and K+ leaks (by 13-16% at 64-400 mM). The effects of ethanol on the Na+,K+ pump and Na+,K+ cotransport system resulted from changes in maximal rates of Na+ efflux (increased and decreased, respectively) without any significant effect on the apparent affinities for internal Na+. Erythrocytes preincubated for 1 hr with 160 mM ethanol, washed and further incubated in flux media, recovered a normal Na+ transport function. In conclusion, high concentrations of ethanol induced reversible perturbations of fluxes catalyzed by erythrocyte Na+ transport systems. The observed effects may reflect disturbances in Na+ transport function associated with severe intoxication.

Biological Transport, Active↗

Chronic alcohol intake induces reversible disturbances on cellular Na+ metabolism in humans: its relationship with changes in blood pressure.

The effect of chronic alcohol consumption on Na(+)-K+ ATPase, Na(+)-Li+ countertransport, outward Na(+)-K(+)-Cl- cotransport system and the Na+ leak was investigated in red blood cells from 18 normotensive subjects with a daily alcohol intake of more than 150 g. The study was repeated after 3 months of alcohol withdrawal, and results were compared with a group of 20 healthy normotensive teetotalers. Maximal efflux rate (Vmax) and apparent dissociation constant for internal Na+ (KNa) of the Na(+)-K+ pump and the Na(+)-Li+ countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and Vmax of both transport systems (p less than 0.05) was observed. These values significantly decreased after alcohol withdrawal. A simultaneous stimulation of the Na(+)-K(+)-Cl- cotransport system after alcohol withdrawal was also observed. Blood pressure values were higher in alcoholics (133.7/82.3) than in abstainers (121.4/75 mmHg) and significantly decreased (128.5/76.9 mmHg) after withdrawal. A positive correlation between the stimulation of the Na(+)-K(+)-Cl- cotransport and the decrease of blood pressure after withdrawal was observed. In conclusion, chronic alcohol intake induces disturbances on red blood cell Na+ metabolism that dissipate with the cessation of drinking. Similar abnormalities also reported in humans and animals with primary hypertension have been associated in the pathogenesis of essential hypertension. Therefore, the pressor effect of chronic alcohol intake could be mediated through these changes in cellular Na+ metabolism.

Adolescent↗

Adult-onset primary open-angle glaucoma caused by mutations in optineurin.

Primary open-angle glaucoma (POAG) affects 33 million individuals worldwide and is a leading cause of blindness. In a study of 54 families with autosomal dominantly inherited adult-onset POAG, we identified the causative gene on chromosome 10p14 and designated it OPTN (for "optineurin"). Sequence alterations in OPTN were found in 16.7% of families with hereditary POAG, including individuals with normal intraocular pressure. The OPTN gene codes for a conserved 66-kilodalton protein of unknown function that has been implicated in the tumor necrosis factor-alpha signaling pathway and that interacts with diverse proteins including Huntingtin, Ras-associated protein RAB8, and transcription factor IIIA. Optineurin is expressed in trabecular meshwork, nonpigmented ciliary epithelium, retina, and brain, and we speculate that it plays a neuroprotective role.

Adult↗

Intracellular forms of simian virus 40 nucleoprotein complexes. I. Methods of isolation and characterization in CV-1 cells.

A new method was developed for isolation of intracellular forms of simian virus 40 (SV40) nucleoprotein complexes from SV40-infected CV-1 cells late in the infectious cycle. In contrast to the Triton extraction method, which yields only a 60-70S complex, this new procedure yielded three forms of SV40 nucleoprotein complexes: complex I, complex II, and the nature virion (V). The three nucleoprotein complexes differed in physical as well as biochemical properties. Complex I, which is only a small portion of the total SV42 nucleoprotein complexes late during infection, was active in synthesizing both SV40-specific DNA and RNA. Pulse-labeling experiments suggest the following metabolic pathway: I leads to II leads to V. Conversion of complex I to II occurred shortly after the completion of SV40 DNA replication and resulted in the inactivation of the biosynthetic activities of I.

Animals↗

Intracellular forms of simian virus 40 nucleoprotein complexes. II. Biochemical and electron microscopic analysis of simian virus 40 virion assembly.

The simian virus 40 virion assembly process was studied with pulse-labeling kinetics of virion proteins, CsCl gradient analysis, electron microscopy, and low-salt gel electrophoresis. The results obtained are consistent with the model of gradual addition and organization of capsid proteins around simian virus 40 chromatin. Empty virions, as observed in the CsCl gradient by previous workers, were found to be the dissociation product of immature virus. Histone H1 was found in simian virus 40 chromatin and virion assembly intermediates but not in the mature virion banding at 1.34 g/ml in the CsCl gradient.

Capsid↗