PubMed Health⌕ Search

Biomedical subjects

A C Adams

Publications and source records attributed to A C Adams.

At least 19 recordsLinked to original sources
PubMed2006

Spitzer spectral observations of the deep impact ejecta.

Spitzer Space Telescope imaging spectrometer observations of comet 9P/Tempel 1 during the Deep Impact encounter returned detailed, highly structured, 5- to 35-micrometer spectra of the ejecta. Emission signatures due to amorphous and crystalline silicates, amorphous carbon, carbonates, phyllosilicates, polycyclic aromatic hydrocarbons, water gas and ice, and sulfides were found. Good agreement is seen between the ejecta spectra and the material emitted from comet C/1995 O1 (Hale-Bopp) and the circumstellar material around the young stellar object HD100546. The atomic abundance of the observed material is consistent with solar and C1 chondritic abundances, and the dust-to-gas ratio was determined to be greater than or equal to 1.3. The presence of the observed mix of materials requires efficient methods of annealing amorphous silicates and mixing of high- and low-temperature phases over large distances in the early protosolar nebula.

Journal Article↗
PubMed2001

Examination of the involvement of protein kinase A in D2 dopamine receptor antagonist-induced immediate early gene expression.

Immediate early genes (IEGs) are induced by different signaling pathways. It has been proposed that D2 dopamine receptor blockade induces IEG expression through activation of protein kinase A (PKA), although few studies have examined this issue in vivo. We infused the PKA inhibitor H-89 into the striatum of male rats, followed 30 min later by systemic administration of eticlopride. Eticlopride-induced c-fos and zif268 mRNA expression in striatum was not blocked by H-89. In addition, eticlopride did not produce measurable levels of PKA activity in striatum, whereas the cAMP activator Sp-8-Br-cAMPs increased levels of activated PKA. Neither the adenosine A2a receptor agonist CGS 21680 nor the phosphodiesterase-4 inhibitor rolipram, each of which should increase PKA activation, potentiated eticlopride-induced IEG expression. To test whether other signaling pathways are involved in eticlopride-mediated gene induction, we also infused inhibitors of the mitogen-activated and calcium/calmodulin-dependent protein kinases into animals and then treated them with eticlopride. The data suggest that eticlopride-induced IEG expression is not solely dependent on these kinases either. These data suggest that PKA activation may not be necessary for induction of IEGs by D2 dopamine receptor antagonists and that other intracellular signaling pathways may be involved.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2000

Degree of immediate early gene induction in striatum by eticlopride determines sensitivity to N-methyl-D-aspartate receptor blockade.

Cortical afferents excite striatal efferent neurons through activation of N-methyl-D-aspartate (NMDA) receptors, which can be modulated by D2 dopamine receptors. It is suggested that activation of PKA by D2 receptor blockade leads to NMDA receptor phosphorylation in the dendrites or phosphorylation of transcription factors in the nucleus. Thus, the levels and cellular localization of activated PKA may determine if D2 antagonist-mediated gene expression is dependent on NMDA receptor activation. We have previously demonstrated that NMDA receptor antagonists block gene expression induced by a high dose of eticlopride in medial and central but not lateral striatum. Here, we examined the effects of NMDA receptor antagonists on striatal gene expression after administration of a low dose of eticlopride. The results showed that NMDA receptor antagonists blocked gene induction by eticlopride throughout striatum. Less PKA activation by the low dose of eticlopride might explain why the expression was more sensitive in the lateral striatum to NMDA receptor blockade than in our previous study. To increase levels of PKA activation to the extent that NMDA receptor blockade would have less effect on eticlopride-mediated gene induction in all regions of striatum, we administered the phosphodiesterase inhibitor IBMX to animals treated with eticlopride. The combined administration of IBMX and eticlopride induced gene expression that was only partially attenuated (c-fos) or unaffected (zif268) by NMDA receptor blockade. These data support the suggestion that the degree of second messenger activation by D2 receptor blockade determines whether D2 dopamine receptor antagonist-mediated gene expression is dependent on NMDA receptor activation.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Effects of conantokins on L-3,4-dihydroxyphenylalanine-induced behavior and immediate early gene expression.

Conantokins, peptides from Conus snails, are N-methyl-D-aspartate (NMDA) receptor antagonists. NMDA receptor antagonists potentiate L-3,4-dihydroxyphenylalanine (L-DOPA)-induced rotation in 6-hydroxydopamine-treated rodents, an index of anti-Parkinsonian potential. This study examined the effects of conantokin-G, conantokin-T(G), CGS 19755, and ifenprodil on L-DOPA-induced contralateral rotation and immediate early gene (IEG) expression in 6-hydroxydopamine-treated rats. Rats received unilateral infusions of 6-hydroxydopamine into the medial forebrain bundle. Three weeks later, rats were treated with an NMDA receptor antagonist, followed by an injection of L-DOPA. Contralateral rotations were recorded for 2 h. In addition, the expression of zif268 and c-fos were examined. Conantokin-G, conantokin-T(G), and CGS 19755 potentiated L-DOPA-induced rotation. Conantokin-G and ifenprodil had no effect on L-DOPA-induced IEG expression, whereas conantokin-T(G) and CGS 19755 attenuated expression. These data suggest that conantokins may be useful in treating Parkinson's disease. Furthermore, different NMDA receptor antagonists have distinct effects on striatal gene expression.

Animals↗
PubMed1999

Buprenorphine potentiates L-DOPA-induced contralateral rotation in 6-hydroxydopamine-treated rats.

Animals are commonly given opioid analgetics such as buprenorphine for post-operative pain management. In this study, the effect of the analgetic buprenorphine, a partial mu receptor agonist and kappa receptor antagonist, on L-DOPA-induced contralateral rotation was measured in 6-hydroxydopamine (6-OHDA) treated rats. Male Sprague-Dawley rats received dopamine-depleting brain lesions by infusion of 6-OHDA into the medial forebrain bundle. After the procedure, buprenorphine was administered (430 microg/kg, s.c.) to 17 of 54 animals. Three weeks after 6-OHDA treatment, animals were given benserazide HCI (25 mg/kg, i.p.) and L-DOPA (4 mg/kg, i.p.). Contralateral rotations were monitored for 2 h. Animals receiving buprenorphine had significantly higher rates of rotation as compared with non-buprenorphine-treated animals (P = 0.023). The results suggest that buprenorphine sensitizes animals to the effects of L-DOPA.

Analgesics, Opioid↗
PubMed1998

Differential effects of N-methyl-D-aspartate receptor blockade on eticlopride-induced immediate early gene expression in the medial and lateral striatum.

The function of striatopallidal neurons is regulated by N-methyl-D-aspartate (NMDA) and dopamine D2 receptors. Previous studies show that immediate early gene induction by D2 receptor blockade is suppressed by NMDA receptor antagonists. Because the pharmacology of NMDA receptors depends on the incorporation of different NR2 subunits and NR2 subunits show regional and cellular differences in their expression in striatum, our study examined whether different NMDA receptor antagonists would have differential effects on eticlopride-induced immediate early gene expression in striatum. Male Sprague-Dawley rats were pretreated with vehicle, CGS 19755, MK-801 or ifenprodil. Rats then received injections of eticlopride and were killed 40 min later. In situ hybridization histochemistry was used to determine the expression of c-fos and zif268 in the striatum. Eticlopride increased immediate early gene expression in striatum, with the increase generally being greater in lateral than in medial striatum. Pretreatment with each of the NMDA receptor antagonists dose-dependently decreased the expression of the immediate early genes. This suppression of eticlopride-induced gene expression was significant only in the medial-central aspect of striatum. Although there was a trend toward suppression of the gene induction in lateral striatum, it did not reach statistical significance and was not typically dose dependent. The data suggest that different types of NMDA receptor antagonists do not exert differential effects on D2 dopamine receptor-mediated function in the striatum. In addition, the data indicate that eticlopride-induced gene expression in the striatum is not uniformly dependent on NMDA receptor activation.

Animals↗
PubMed1997

The cyanobacterial repressor SmtB is predominantly a dimer and binds two Zn2+ ions per subunit.

The Synechococcus PCC7942 metallothionein repressor gene smtB has been cloned into a high expression vector and the protein purified to near homogeneity (>/=98%). Analytical ultracentrifugation studies demonstrate that the protein is predominantly dimeric in 0.1 M NaCl, pH 7.4, and 22 degrees C, exhibiting a monomer-dimer-tetramer equilibrium. The monomer-dimer (Ka(1,2)) and the dimer-tetramer (Ka(2,4)) association constants are 3.24 x 10(5) and 9.90 x 10(2) M-1, respectively. The repressor binds two Zn2+ ions per subunit with an overall Kd of 3.49 x 10(-6) M. In the presence of Zn2+, Ka(1, 2) increases by 2 orders of magnitude to 1.25 x 10(7) M-1 and the apparent weight-averaged sedimentation coefficient increases from 2. 00 to 2.22 S. The fact that the increase in sedimentation coefficient is greater than that predicted by increased dimerization is interpreted as caused by compaction of the structure in the presence of metal ions. At pH 6.0, 0.1 M NaCl, and 22 degrees C, the protein exhibits only a monomer-dimer equilibrium, with Ka(1,2) = 1.52 x 10(7) M-1 which is almost identical to that seen upon binding Zn2+ at pH 7.4. The compaction and conformational change in SmtB caused by Zn2+ is consistent with a role for this altered quaternary state in derepression of smtA in Synechococcus challenged with heavy metal ions.

Bacterial Proteins↗
PubMed1996

Cyanobacteria carrying an smt-lux transcriptional fusion as biosensors for the detection of heavy metal cations.

The metal-responsive smt operator/promoter region of Synechococcus PCC7942 was fused to the luxCDABE genes of Vibrio fischeri. Plasmid DNA (pJLE23) carrying this fusion conferred metal ion-inducible luminescence to transformed cyanobacteria. Synechococcus PCC7942 (pJLE23) was sensitive to ZnCl2 concentrations within a range of 0.5-4 microM as demonstrated by induction of luminescence. Trace levels of CuSO24 and CdCl2 were also detected.

Bacterial Proteins↗
PubMed1995

Dementia: diagnosis and evaluation.

OBJECTIVE: To describe an approach to the diagnosis of dementia based on effective assessment methods. DESIGN: We reviewed the literature and summarized the available diagnostic and prognostic studies of dementia that may be useful to the primary-care physician. RESULTS: Although controversy exists about certain aspects of the diagnostic workup, exclusion of potentially reversible causes of dementia is essential. Laboratory studies (for example, for detection of underlying metabolic abnormalities) and neuroimaging of the brain may be useful. The pattern of onset and the temporal course of the disease may suggest a cause and help direct the investigation. Functional losses can substantially impair the patient's ability to live independently. CONCLUSION: Dementia can be mistakenly considered as part of the normal aging process, and diagnosis necessitates a thorough, although not exhaustive, approach. Early identification of dementing illnesses improves the outcome for reversible disease and may also enhance the management of incurable dementias.

Dementia↗
PubMed1977

Immunization of mice against Naegleria fowleri infection.

Naegleria fowleri produces fatal meningoencephalitis in humans and in experimentally infected laboratory animals. The course of the disease in mice is dependent upon the infecting dose of amoebae, route of inoculation, and prior exposure to Naegleria antigens. DUB/ICR mice were immunized by various routes and antigen preparations, held for 21 days, and, together with noninfected control mice, challenged intravenously (i.v.) or intranasally (i.n.) with 10(7) or 10(6) N. fowleri per mouse, respectively. Mice immunized with liver or formalinized N. fowleri or live N. gruberi subcutaneously, intraperitoneally, i.v., or i.n. were significantly protected against a subsequent lethal challenge with N. fowleri i.v. or i.n. In general, i.v. inoculation afforded greated protection than other routes of immunization, intact cells immunized mice better than did cell fragments, and N. gruberi appeared to be a better immunogen than N. fowleri.

Administration, Intranasal↗
PubMed1976

Enhanced toxicity for mice of combinations of bacterial lipopolysaccharide and vincristine.

Sublethal doses of vincristine (VNC) and bacterial lipopolysaccharide (LPS) administered simultaneously to adult male mice resulted in markedly enhanced mortality. All of 10 strains of Pseudomonas aeruginosa tested, 4 of 7 strains of Bacteroides, and 6 of 10 strains of Listeria monocytogenes were able to substitute for purified LPS in enhancing mortality in VNC-treated mice. Inoculation of mice with each of 10 strains of Pseudomonas, each of 7 strains of Bacteroides, and about half of the 10 strains of Listeria tested elicited increased resistance to the lethal action of purified LPS. The patterns of responses of mice receiving a lethal combination of 2 mg of LPS/kg and 1 mg of VNC/kg resembled those of mice receiving a lethal dose of 10 mg of VNC/kg alone or 15 mg of LPS/kg alone with respect to (i) serum glutamic pyruvate transaminase activity, (ii) hematocrit values, and (iii) thrombocytopenia. The patterns of responses of mice receiving a lethal combination of LPS and VNC resembled those of mice receiving a lethal dose of LPS alone with respect to (i) hypothermia, (ii) retention of sulfobromophthalein, (iii) fibrinogen level, (iv) prothrombin activity, (v) blood urea nitrogen levels, and (vi) time of death. These data are consistent with the proposition that the combination of VNC and LPS produces a fatal renal failure. Histological studies confirmed that there was extensive renal damage in mice treated with lethal doses of LPS alone or a lethal combination of LPS and VNC.

Animals↗
PubMed1976

Modification of resistance of mice to Naegleria fowleri infections.

Naegleria fowleri, which produces a fatal meningoencephalitis in humans, is also able to produce a progressive and fatal disease in mice. The course of the disease in DUB/ICR mice is dependent upon the infecting dose of organisms, whether administered intraperitoneally (i.p.) or intravenously (i.v.). All of the mice receiving 10(7) trophozoites/mouse i.v. or 4.85 X 10(7) trophozoites/mouse i.p. were killed within 10 days. Escherichia coli O26:B6 lipopolysaccharide, administered at a dose of 1 mg/kg 24 h prior to N. fowleri, afforded some protection for several days after challenge, but by day 8 there was no difference in survival of untreated and endotoxin-treated mice. No significant protection was afforded by a complex of lipid A with concanavalin A (ConA) or bovine serum albumin (BSA) or by dimethylmyristamide-BSA, dimethylmyristamide, BSA, beta-hydroxymyristic acid-ConA, beta-hydroxymyristic acid, ConA, myristic acid-BSA, or myristic acid. Mice surviving primary i.v. or i.p. challenge doses of N. fowleri, 5 X 10(6) and 10(7) trophozoites/mouse, respectively, were highly resistant to rechallenge with an i.v. dose of organisms (5 X 10(6) Naegleria/mouse) that produced uniformly fatal disease in untreated control mice.

Amoeba↗
PubMed1975

Potentiation of the toxicity of mithramycin by bacterial lipopolysaccharide.

The lethality for BALB/c mice of 1,3-bis(2-chloroethyl)-1-nitrosourea, cytosine arabinoside, 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea, hydroxyurea, mithramycin, a polymyxin-like antibiotic (SQ 21,286), polyadenylic polyuridylic acid, procarbazine, 5-[3,3-bis(2-chloroethyl)-1-triazeno]-imidazole-4-carboxamide (TIC-mustard) or uracil arabinoside administered in combination with Escherichia coli lipopolysaccharide (LPS) was measured. Simultaneously administered mithramycin and LPS or TIC-mustard administered 24 h after LPS synergistically killed mice. Concanavalin A potentiated the lethality of TIC-mustard but not of eight other drugs tested. Pretreatment of mice with LPS or lipid A complexed to concanavalin A rendered mice resistant to the lethal action of LPS alone or combinations of LPS and mithramycin. Mithramycin-treated mice were killed by minute amounts of LPS. Mice sensitized to LPS by mithramycin were used to detect endotoxic activity in biological materials, such as commercially available enzymes, and in a complex of lipid A with concanavalin A.

Animals↗