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Biomedical subjects

M A Cook

Publications and source records attributed to M A Cook.

At least 37 records · Page 2Linked to original sources
PubMed1996

Primary skeletal lymphoma imaging and pathologic correlation.

Primary skeletal lymphoma is an uncommon tumor whose appearance on plain-film radiographs has been well described. However, few reports have described the appearance of this neoplasm on magnetic resonance imaging. As in the primary skeletal lymphoma described, magnetic resonance imaging can be used to define the extent of the tumor and the degree of soft tissue and bone marrow involvement. It can also help to determine the biopsy site and to monitor the tumor's response to radiation therapy.

Adult↗
PubMed1994

Boomerang pillows and respiratory capacity.

An experimental study was done to determine whether subjects placed on boomerang pillows would have lower vital capacities than subjects placed on straight pillows after 30 minutes. A sample of 42 subjects took part in the study in a nursing laboratory. A crossover design was used in which subjects were measured in both conditions. The findings indicated that there was no significant difference in the vital capacities of subjects in the two conditions. An associated finding was that the vital capacities were significantly lower in a semi-Fowler's position than in a straight chair. It was concluded that boomerang pillows are safe to use for persons without respiratory problems. Further research is needed into the effect of boomerang pillows on persons with respiratory deficits.

Bedding and Linens↗
PubMed1994

Neurocysticercosis: an old disease with new questions.

Cysticercosis is a parasitic infection of the central nervous system that occurs in some geographic regions and is transmitted through contaminated food or by the fecal-oral route. Treatment depends on the degree of central nervous system involvement. Ventricular cysts require surgery. Parenchymal involvement requires systemic antiparasitic therapy. Computed tomography and magnetic resonance imaging are used to image patients with neurocysticercosis. Magnetic resonance imaging is more sensitive for cerebral involvement than in computed tomography. Computed tomography is more sensitive to calcifications than is magnetic resonance imaging.

Brain Diseases↗
PubMed1993

PYY: a neuropeptide in the canine enteric nervous system.

This study re-examined the anatomical locations of PYY in the canine gastrointestinal tract. Immunohistochemical studies with two relatively selective PYY antisera demonstrated PYY-LI immunoreactivity in nerve cell bodies and nerve fibres in the intestinal and gastric myenteric plexus and the intestinal submucosal plexus and in nerve fibres of the intestinal deep muscular plexus. Immunoreactive PYY-LI was also present in ileal endocrine cells. All PYY-LI immunoreactivity was completely abolished by pre-incubation of the antibodies with synthetic PYY but was unaltered by pre-incubation with synthetic NPY. Individual synaptosomal preparations obtained from canine intestinal and gastric myenteric plexus, and intestinal deep muscular plexus and submucous plexus, contained considerable quantities of PYY-LI which, on reverse-phase HPLC, co-eluted with a synthetic canine/porcine PYY standard. In contrast, isolated myenteric ganglia from rat and guinea pig did not contain detectable amounts of PYY-LI. These studies demonstrate that PYY is not confined to distal intestinal endocrine cells in the dog but is also an enteric neuropeptide with maximal concentrations being present in the intestinal myenteric plexus.

Animals↗
PubMed1993

Adenosine and 5-HT inhibit substance P release from nerve endings in myenteric ganglia by distinct mechanisms.

Release of substance P-like immunoreactivity (SP-LI) from dissociated enteric ganglia and the receptor-mediated prejunctional inhibition of this release were investigated with the use of a perifusion technique. SP-LI release was evoked by elevated extracellular K+ concentration and was inhibited, in a graded manner, by N6-cyclopentyl adenosine (CPA), an adenosine analogue with selectivity for adenosine A1 receptors. Similar inhibition of SP-LI release was obtained with 5-hydroxytryptamine (5-HT); incrementing concentrations, however, yielded a biphasic concentration-response relationship. The selective adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentyl-xanthine abolished the inhibition due to CPA, whereas the inhibitory action of 5-HT was sensitive to the 5-HT1A-selective antagonist 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]-piperazine hydrobromide. Inhibition due to both agonists was insensitive to blockade by tetrodotoxin, suggesting a prejunctional locus for both adenosine and 5-HT1A receptors on the tachykininergic nerve endings. Pretreatment of ganglia with pertussis toxin had no effect on CPA-mediated inhibition of SP-LI release, whereas 5-HT-mediated inhibition was abolished. The findings demonstrate that adenosine and 5-HT receptors on enteric nerve endings are coupled to inhibition of tachykinin release through distinct mechanisms, putatively distinct G proteins.

Adenosine↗
PubMed1993

Inhibition of neurotransmitter release from enteric nerve endings by 2-[p-(carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamido-adenosine (CGS-21680) and related adenosine analogs: lack of simple competition by antagonists.

Adenosine receptors on enteric nerves mediate inhibitory responses to adenosine and its analogs and contribute to the overall excitability of enteric nerves. In characterizing these receptors, the response of the electrically stimulated guinea pig ileum longitudinal muscle-myenteric plexus preparation to receptor-selective analogs of adenosine was investigated and the antagonism of such activity by selective antagonists quantitated. The A1-selective agonist N6-cyclopentyladenosine, the nonselective agonist 5'-N-ethylcarboxamidoadenosine and the 2-substituted uronamides, 2-[p-(carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenosine and 2-[-(4-fluorophenyl)-ethoxy]-5'-N-ethylcarboxamidoadenosine, both relatively A2-selective agonists, inhibited field-stimulated responses of the ileum with the potency rank order: N6-cyclopentyladenosine > 5'-N-ethylcarboxamidoadenosine >> 2-[p-(carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenosine approximately 2-[-(4-fluorophenyl)-ethoxy]-5'-N-ethylcarboxamidoadenosine. Antagonism of these responses by receptor-selective antagonists was quantitated using the Schild technique and, for 1,3-dipropyl-8-cyclopentylxanthine, the A1-selective antagonist, demonstrated simple competitive interaction with the responses to N6-cyclopentyladenosine yielding a linear Schild isobole with unit slope. In contrast, responses to the uronamides could not be antagonized in a simple competitive manner. The potency order of the selective agonists is compatible with the presence on enteric nerve endings of an A1 receptor but does not support the presence of the A2 subtype. Moreover, these data demonstrate that the putatively A2-selective adenosine analogs 2-[p-(carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamidoadenosine and 2-[-(4-fluorophenyl)-ethoxy]-5'-N-ethylcarboxamidoadenosine interact with 1,3-dipropyl-8-cyclopentylxanthine at enteric nerve adenosine receptors in a manner which is not compatible with simple competitive interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Group C streptococcal arthritis.

Septic arthritis is a common disorder that is rarely caused by group C streptococci. This infectious process usually occurs in patients with a preexisting rheumatologic condition. Treatment consists of intravenous antibiotics, joint aspiration, and physical therapy. Prolonged recovery and septic complications are expected. This report describes a case typical of group C streptococcal arthritis.

Arthritis, Infectious↗
PubMed1992

Adenosine A1 receptors mediate inhibition of tachykinin release from perifused enteric nerve endings.

A perifused preparation of guinea pig myenteric nerve varicosities (synaptosomes) was used to determine the characteristics of evoked tachykinin release and the inhibition of such release by adenosine analogues. Release of substance P-like immunoreactivity (SP-LI) and neurokinin A-like immunoreactivity (NKA-LI) was evoked by elevated extracellular [K+] in a reversible and repeatable manner. This release was completely abolished in the absence of extracellular Ca2+. Perifusion in the presence of 5'-N-ethylcarboxamidoadenosine (NECA), a nonselective A1/A2 adenosine receptor agonist, decreased K(+)-evoked release of SP-LI and NKA-LI compared with that in the absence of the nucleoside. Similar decrements in peptide release were obtained with N6-cyclopentyl adenosine (CPA), a selective A1 agonist, and 2-[p-(2-carboxyethyl)]phenethylamino-5'-N-ethyl-carboxamidoadenosi ne (CGS 21680), a selective A2 agonist. Response to all nucleosides was graded. Potency order of adenosine analogues was CPA greater than NECA much greater than CGS 21680. Inhibition due to the nucleosides was diminished in the presence of the highly selective A1-receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) while perifusion in the presence of DPCPX alone did not alter evoked release of either peptide. These findings provide direct measurements of inhibitory effects of adenine nucleosides on the release, from enteric nerve endings, of endogenous neuromediators SP and NKA. The findings also directly demonstrate the presence of functional adenosine receptors of the A1 subtype on enteric nerve endings coupled negatively to release of tachykinins. The presence of A2 receptors on enteric nerve endings is neither supported nor excluded.

Adenosine↗
PubMed1992

Adenosine A1 receptor activation attenuates cardiac injury produced by hydrogen peroxide.

Adenosine has been shown to protect the ischemic and reperfused myocardium. To examine whether the protective effect of the nucleoside is mediated by modulation of oxidative stress, isolated rat hearts were perfused for 30 minutes with 100 microM H2O2 or an exogenous free radical-generating system consisting of purine (3.06 mM) and xanthine oxidase (10 units/l) in the presence or absence of drugs acting on adenosine A1 or A2 receptors. H2O2 alone produced a greater than 90% loss in contractility concomitant with a threefold elevation in resting tension, although these effects occurred in the absence of ultrastructural damage. Two A1 receptor agonists N6-cyclopentyladenosine (CPA, 1 microM) and R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA, 1 microM) significantly attenuated the cardiodepressant effects of H2O2 and depressed the elevation in resting tension; however, only the effect of CPA was found to be significant with regard to the latter parameter. A similar concentration of S(+)-N6-(2-phenylisopropyl)adenosine (S-PIA), a markedly less potent A1 receptor agonist, was found to be without beneficial effect. However, a significant protective effect against both the reduction in contractility and the elevation in resting tension was seen with a 10-fold elevation in the concentration of S-PIA (10 microM). The protective effects on functional parameters were associated with preservation of high-energy phosphate and adenine nucleotide contents after 30 minutes of H2O2 treatment. The salutary effects of all drugs were reversed in the presence of the A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (0.5 microM). An A2 receptor agonist 2-[p-(carboxyethyl)phenethylamino]-5'-N-ethylcarboxamidoadenosine, termed CGS 21680 (1 microM), failed to alter the cardiac response to H2O2 with regard to all parameters studied. Neither a 50% reduction in external CaCl2 concentration nor treatment with 10 microM DL-propranolol exerted salutary effects against H2O2-induced dysfunction. None of the A1 receptor agonists modulated the response to purine plus xanthine oxidase. Our results demonstrate a selective protective effect of adenosine A1 receptor activation against the cardiac toxicity of H2O2 and provide, at least in part, a basis for the cardioprotective actions of adenosine and its analogues.

Adenosine↗
PubMed1990

Neuropeptide release from isolated myenteric nerve endings derived from the guinea pig myenteric plexus.

Isolated myenteric nerve varicosities prepared from the myenteric plexus of the guinea pig ileum were investigated as a suitable model system with which to study the release of several neuropeptide-like immunoreactivities (-LI). Basal release of substance P-LI, neurokinin A-LI, Leu-enkephalin-LI and Met-enkephalin-LI was determined, and clear depolarization-induced release of the enkephalin-LI's and neurokinin A-LI was obtained using this preparation, providing further support for their roles as putative mediators in the enteric nervous system. Evoked-release of these peptides was dependent on the presence in the incubation mixture of certain antagonists to known endogenous neuronal mediators. In the absence of such antagonists, no unequivocal evidence of release was seen. Clear evoked release of Leu-enkephalin-LI occurred only in the presence of the adenosine receptor antagonist 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX), atropine and naloxone. Release of Met-enkephalin-LI occurred in the presence of either atropine or naloxone. The release of neurokinin A-LI was evident in the presence of DPSPX. These findings suggest the existence of either distinct subpopulations of nerve varicosities or distinct neuronal pools containing each peptide and that these peptides may be under differential regulation by endogenous inhibitory mediators. It is concluded that, under suitable conditions, isolated myenteric nerve varicosities provide a useful model system for the study of release, and the modulation of release, of endogenous neuropeptides.

Animals↗
PubMed1990

Adenosine receptors are coupled negatively to release of tachykinin(s) from enteric nerve endings.

Adenosine receptors capable of modulating tachykininergic transmission were characterized in functional studies using both field-stimulated and cholecystokinin octapeptide-stimulated contractile responses of atropinized guinea pig longitudinal muscle-myenteric plexus preparations. These tetrodotoxin-sensitive responses, which were mediated by release of one or more tachykinins, were inhibited by adenosine analogs in a concentration-dependent manner. The rank order of potencies of the analogs as inhibitors of the responses to cholecystokinin octapeptide was N6-cyclopentyladenosine greater than 5'-N-ethylcarboxamidoadenosine much greater than 2-phenylaminoadenosine (CV 1808). Schild analysis of the antagonism of the presynaptic inhibitory effects of 5'-N-ethylcarbocamidoadenosine and N6-cyclopentyladenosine on cholecystokinin octapeptide-stimulated responses using the A1 selective antagonists 1,3-dipropyl-8-(4-sulfophenyl)xanthine and 1,3-dipropyl-8-(cyclopentyl)xanthine yielded linear isoboles with unit slopes indicating competitive antagonism. The affinity of the antagonists for the receptor site(s) involved in inhibition of tachykininergic transmission was similar to those established previously for cholinergic transmission. The rank order of potency of adenosine analogs as inhibitors of the field-stimulated responses was such that N6-cyclopentyladenosine = 5'-ethylcarboxamidoadenosine. Reverse-phase high-performance liquid chromatography analysis performed on lysates of isolated myenteric nerve endings demonstrated the presence of substance P and neurokinin-A. Neurokinin-B was undetectable. These studies indicate that adenosine receptor(s) on myenteric nerve endings are coupled negatively to tachykinin release and that they are probably identical to those involved in the modulation of acetylcholine release.

Acetylcholine↗
PubMed1988

Characterization of content and chromatographic forms of neuropeptides in purified nerve varicosities prepared from guinea pig myenteric plexus.

Partially purified nerve varicosities (PV) prepared from guinea pig ileal myenteric plexus were found to contain, by radioimmunoassay, gastrin-releasing polypeptide (GRP), substance P (SP), galanin, Leu-enkephalin (LE), Met-enkephalin (ME), and vasoactive intestinal polypeptide (VIP). SP was present in the highest concentration followed by, in descending order, ME, LE, VIP, GRP and galanin. On reverse-phase HPLC, SP-, LE- and ME-like immunoreactivity in the PV preparation eluted at retention times similar to their synthetic analogues, galanin-like immunoreactivity eluted at a retention time different from that of synthetic porcine galanin and VIP-like immunoreactivity eluted at the retention time of synthetic guinea pig VIP. GRP-like immunoreactivity, on reverse-phase HPLC, eluted at retention times close to that of synthetic porcine GRP-(1-27) and its major oxidized form. Evidence was obtained for the presence of an alpha-neurokinin-like immunoreactive entity and an unidentified SP-like immunoreactive entity in guinea pig myenteric plexus.

Animals↗