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Biomedical subjects

R E Blair

Publications and source records attributed to R E Blair.

11 recordsLinked to original sources
PubMed2000

Measurement of J/psi and psi(2S) polarization in pp collisions at sqrt[s] = 1.8 TeV.

We have measured the polarization of J/psi and psi(2S) mesons produced in pp collisions at sqrt[s] = 1.8 TeV, using data collected at the Collider Detector at Fermilab during 1992-1995. The polarization of promptly produced J/psi [psi(2S)] mesons is isolated from those produced in B-hadron decay, and measured over the kinematic range 4 [5.5]<P(T)<20 GeV/c and |y|<0.6. For P(T) greater than or approximately equal 12 GeV/c we do not observe significant polarization in the prompt component.

Journal Article↗
PubMed2000

Search for scalar top and scalar bottom quarks in pp collisions at square root s=1.8 TeV.

We have searched for direct pair production of scalar top and scalar bottom quarks in 88 pb-1 of pp collisions at sqrt[s]=1.8 TeV with the CDF detector. We looked for events with a pair of heavy flavor jets and missing energy, consistent with scalar top (bottom) quark decays to a charm (bottom) quark and a neutralino. The numbers of events that pass our selections show no significant deviation from standard model expectations. We compare our results to the next-to-leading order scalar quark production cross sections to exclude regions in scalar quark-neutralino mass parameter space.

Journal Article↗
PubMed2000

Search for a W' boson via the decay mode W'-->munumu in 1.8 TeV pp collisions.

We report the results of a search for a W' boson produced in pp collisions at a center-of-mass energy of 1.8 TeV using a 107 pb-1 data sample recorded by the Collider Detector at Fermilab. We consider the decay channel W'-->&munumu and search for anomalous production of high transverse mass munumu lepton pairs. We observe no excess of events above background and set limits on the rate of W' boson production and decay relative to standard model W boson production and decay using a fit of the transverse mass distribution observed. If we assume standard model strength couplings of the W' boson to quark and lepton pairs, we exclude a W' boson with invariant mass less than 660 GeV/c2 at 95% confidence level.

Journal Article↗
PubMed1999

Long-lasting decrease in neuronal Ca2+/calmodulin-dependent protein kinase II activity in a hippocampal neuronal culture model of spontaneous recurrent seizures.

Ca2+/calmodulin-dependent protein kinase II (CaM Kinase II) activity was evaluated in a well-characterized in vitro model of epileptiform activity. Long-lasting spontaneous recurrent seizure (SRS) activity was induced in hippocampal neuronal cultures by exposure to low Mg2+ media for 3 h. Analysis of endogenous Ca2+/calmodulin-dependent phosphorylation revealed a significant long-lasting decrease in 32P incorporation into the alpha (50 kDa) and beta (60 kDa) subunits of CaM kinase II in association with the induction of SRS activity in this preparation. Ca2+/calmodulin-dependent substrate phosphorylation of the synthetic peptides, Autocamtide-2 and Syntide II, was also significantly reduced following the induction of SRSs and persisted for the life of the neurons in culture. The decrement in CaM kinase II activity associated with low Mg2+ treatment remained significantly decreased when values were corrected for changes in levels of alpha subunit immunoreactivity and neuronal cell loss. Addition of the protein phosphatase inhibitors, okadaic acid and cyclosporin A, to the phosphorylation reaction did not block the SRS-associated decrease in substrate phosphorylation, indicating that enhanced phosphatase activity was not a contributing factor to the observed decrease in phosphate incorporation. The findings of this study demonstrate that CaM kinase II activity is decreased in association with epileptogenesis observed in these hippocampal cultures and may contribute to the production and maintenance of SRSs in this model.

Animals↗
PubMed1992

Enhanced suppression of humoral immunity in DBA/2 mice following subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Previous studies have indicated that mice which differ in their acute susceptibility to responses mediated by the Ah receptor have a pattern of suppression of the antibody response which is consistent with a role by the putative dioxin receptor. The objective of the present investigation was to compare the TCDD-induced suppression of the antibody response following acute and subchronic exposures in B6C3F1 mice, an Ah-high-responder strain, and DBA/2 mice, an Ah-low-responder strain. Results of our initial studies demonstrate that suppression of humoral immunity can be enhanced in DBA/2 mice approximately 10-fold following subchronic versus acute exposures to the same cumulative doses of TCDD. This change in suppression of the antibody response in DBA/2 mice was not accompanied by significant changes in liver weight (hepatomegaly), as was observed in the B6C3F1 strain when exposed under comparable conditions. In contrast, effects on thymus weight (involution) were enhanced in the DBA/2 mice following subchronic exposure and demonstrated a higher degree of atrophy than was seen in the B6C3F1 strain (68 versus 56% decrease in thymic weight at the 42 micrograms/kg cumulative dose). These findings suggest that multiple mechanisms may be operating to suppress humoral immunity in vivo and that the conditions of exposure can alter the toxic effects of TCDD in the DBA/2, Ah-low responsive, mouse strain.

Animals↗
PubMed1990

Temperature modulation of ischemic neuronal death and inhibition of calcium/calmodulin-dependent protein kinase II in gerbils.

We used brief bilateral carotid artery occlusion in gerbils to examine the effects of temperature on ischemia-induced inhibition of calcium/calmodulin-dependent protein kinase II activity and neuronal death. In normothermic (36 degrees C) gerbils, ischemia induced a severe loss of hippocampal CA1 pyramidal neurons measured 7 days after ischemia (28.4 neurons/mm, n = 10; control density in 10 naive gerbils 262.1 neurons/mm) and a significant decrease in forebrain calcium/calmodulin-dependent protein kinase II autophosphorylation measured 2 hours after ischemia (12.9 fmol/min, n = 6; control phosphorylation in six naive gerbils 23.5 fmol/min). The effect of temperature on these indicators of ischemic damage was examined by adjusting intracerebral temperature before and during the ischemic insult. Hyperthermic (39 degrees C) gerbils showed almost complete loss of neurons in the CA1 region (3.0 neurons/mm, n = 11) and extension of neuronal death into the CA2, CA3, and CA4 regions. In addition, hyperthermia exacerbated ischemia-induced inhibition of calcium/calmodulin-dependent protein kinase II activity (4.2 fmol/min, n = 6). Hypothermia (32 degrees C) protected against ischemia-induced CA1 pyramidal cell damage (257.0 neurons/mm, n = 20) and inhibition of calcium/calmodulin-dependent protein kinase II activity (26.0 fmol/min, n = 6). Our results are consistent with the hypothesis that loss of calcium/calmodulin-dependent protein kinase II activity may be a critical event in the development of ischemia-induced cell death.

Animals↗
PubMed1989

Phenytoin protects against ischemia-produced neuronal cell death.

Brief bilateral carotid occlusion in the gerbil produces forebrain ischemia that results in almost complete neuronal destruction in the CA1 sector of the hippocampus. Treatment with phenytoin (200 mg/kg) blocked the ischemia-induced neuronal death. The average density of CA1 pyramidal neurons (cells/mm CA1) was 253.6 +/- 4.4 in the sham surgery group, 12.3 +/- 3.4 in the ischemia group, and 119.5 +/- 16.6 in the group treated with phenytoin before ischemia. Thus, phenytoin reduced ischemia-produced neuronal loss in hippocampal CA1 by 44.4% (P less than 0.001). The plasma levels of phenytoin that produced this effect ranged from 28.1 to 45.0 mg per liter, with a mean phenytoin level of 34.7 +/- 1.7 mg/l (n = 10). The results suggest that phenytoin may be a clinically useful cerebroprotective agent.

Animals↗
PubMed1989

Conditions for pharmacologic evaluation in the gerbil model of forebrain ischemia.

We looked at FiO2, choice of anesthetic, nutritional status, and body temperature in a gerbil model of forebrain ischemia to determine their effect on data interpretation, ischemic outcome, and extent of pharmacologic protection. We subjected 484 gerbils to 5 minutes of forebrain ischemia under different experimental conditions. The gerbils were anesthetized with 3% halothane and inspired 21% O2, 37% O2 and 60% N2O, or 97% O2. Six groups of gerbils pretreated with 200 mg/kg phenytoin or 2 ml/kg polyethylene glycol (vehicle) underwent ischemia in the fasted or fed state. Three groups of gerbils receiving no pretreatment underwent ischemia with rectal temperatures of 32-33 degrees C, 34-35 degrees C, or 37 degrees C. We counted intact neurons in the CA1 hippocampal sector in brains fixed on Day 7 after ischemia. t tests of square-root-transformed cell counts were used to assess the effect of hypothermia, and analysis of variance of the transformed data was used to test for the effects of phenytoin, FiO2, and nutritional status. Phenytoin pretreatment provided significant protection from CA1 neuron loss in all groups tested (p less than 0.001), but the degree of protection varied from 20% to 44%. In spite of significantly higher serum glucose concentrations in fed than in fasted gerbils (173 and 118 mg/dl, respectively), we found no significant effect of nutritional status upon neuron loss in phenytoin- or vehicle-pretreated gerbils. An FiO2 of 21% significantly decreased the number of viable neurons in both vehicle- and phenytoin-pretreated groups (p less than 0.03), despite the lack of an effect of hypoxemia on arterial blood gases.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1988

Cerebral ischemia decreases endogenous calcium-dependent protein phosphorylation in gerbil brain.

Acute forebrain ischemia in the gerbil produced a significant decrease in endogenous Ca2+-dependent hippocampal protein phosphorylation in comparison to sham and naive control animals. Inhibition of Ca2+-dependent phosphorylation was demonstrated as early as 2 h post-ischemia and shown to persist up to 7 days following the ischemic insult. The ischemia-induced loss of Ca2+-dependent phosphorylation was only seen in brain regions affected by the localized ischemia and not in non-ischemic brain regions from the same animal. These results suggest that an early event in the development of ischemia-induced neuronal death is a decrease in Ca2+-dependent protein phosphorylation.

Animals↗
PubMed1981

Pets, pica, pathogens and pre-school children.

The incidence of pica in pre-school children was investigated by studying 192 children attending a general paediatric hospital clinic and 69 attending a general practice surgery. The incidence of pica was twice as common in those who kept pets in both study groups. Half of the pet-keeping children with pica had eaten their pet's food. Imitative behaviour is suggested as a probable cause. Pet-keeping compounds a child's risk of infestation not only by providing close contact with a reservoir of enteropathogens but also by encouraging pica.

Animal Feed↗