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S F Moore

Publications and source records attributed to S F Moore.

13 recordsLinked to original sources
PubMed1999

Alterations in calcium-mediated signal transduction after traumatic injury of cortical neurons.

Calcium influx and elevation of intracellular free calcium ([Ca2+]i), with subsequent activation of degradative enzymes, is hypothesized to cause cell injury and death after traumatic brain injury. We examined the effects of mild-to-severe stretch-induced traumatic injury on [Ca2+]i dynamics in cortical neurons cultured on silastic membranes. [Ca2+]i was rapidly elevated after injury, however, the increase was transient with neuronal [Ca2+]i returning to basal levels by 3 h after injury, except in the most severely injured cells. Despite a return of [Ca2+]i to basal levels, there were persistent alterations in calcium-mediated signal transduction through 24 h after injury. [Ca2+]i elevation in response to glutamate or NMDA was enhanced after injury. We also found novel alterations in intracellular calcium store-mediated signaling. Neuronal calcium stores failed to respond to a stimulus 15 min after injury and exhibited potentiated responses to stimuli at 3 and 24 h post-injury. Thus, changes in calcium-mediated cellular signaling may contribute to the pathology that is observed after traumatic brain injury.

Animals↗
PubMed1997

The biodisposition and metabolism of anandamide in mice.

The endogenous cannabinoid anandamide (AN) has been reported to produce pharmacological effects similar to those of delta9-tetrahydrocannabinol but with a shorter duration of action. Also, AN is known to be metabolized to arachidonic acid. The purpose of this study was to examine the time course of distribution and metabolism of AN. Male mice were each administered 20 microCi 3H-AN and 50 mg/kg AN (i.v.). At 1, 5, 15 and 30 min after administration, the animals were sacrificed, and various tissues were removed, solubilized and counted to determine the distribution of 3H. Also, samples from brain, adrenal gland and plasma were extracted with ethyl acetate and analyzed by HPLC to separate 3H-labeled AN, arachidonic acid and other metabolites. AN was detectable in brain by 1 min after injection. At 1 min after injection, the rank order of radioactivity per milligram or microliter of tissue was adrenal > lung > kidney > plasma > heart > liver > diaphragm > brain > fat. Although the 1 and 5 min metabolic profiles of brain 3H showed that AN was clearly present, most AN had already been transformed to arachidonic acid and other polar metabolites, and there were almost no detectable brain levels of AN at 15 and 30 min. In plasma and adrenal gland, AN was the predominant form at 1 and 5 min. Our experiments confirm that AN quickly reaches the brain and suggest that rapid metabolism of AN plays a key role in the time course of the pharmacological activity of this naturally occurring cannabinoid receptor ligand.

Animals↗
PubMed1995

Endothelial and nonendothelial cyclooxygenase mediate rabbit pial arteriole dilation by bradykinin.

Aspirin (acetylsalicylic acid, ASA) was administered to rabbits in an attempt to inhibit selectively endothelial cyclooxygenase activity and therefore to determine its role in bradykinin-induced radical-mediated dilation of cerebral arterioles. With the use of the cranial window technique in anesthetized rabbits, pial arteriolar diameters were recorded in response to topically applied bradykinin, acetylcholine, and ventilation with 10% O2-9% CO2 gas mixture. Prostaglandins were measured in isolated cerebral microvessels and cerebrospinal fluid (CSF) using radioimmunoassay. Microvessel prostaglandin production was reduced significantly by 90 mg/kg i.v. ASA, whereas acetylcholine-stimulated increases of CSF prostaglandins were not similarly affected. This treatment reduced bradykinin-induced dilation of pial arterioles by 47%. After concurrent 90 mg/kg i.v. ASA plus 300 microM ASA topically applied to the brain, stimulated increases of CSF prostaglandins were reduced by 79%, while bradykinin-induced dilation was reduced by 78%. ASA did not reduce the dilator activity of either acetylcholine or ventilation with 10% O2-9% CO2. Acetylcholine- but not bradykinin-induced dilation was reduced by NG-nitro-L-arginine methyl ester. These results indicate intravenous ASA produced a relatively selective inhibition of cerebral microvascular cyclooxygenase and partial inhibition of bradykinin-induced dilation. Further inhibition of dilation occurred following ASA administered both systemically and topically to the brain. This indicates two sources of cyclooxygenase, endothelial and nonendothelial, mediate the bradykinin-induced dilation of rabbit pial arterioles. Furthermore, systemic doses of ASA do not eliminate brain prostaglandin formation.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Anandamide and delta 9-THC dilation of cerebral arterioles is blocked by indomethacin.

Anandamide (AN, arachidonyl ethanolamide) has been isolated from the brain and shown to be an endogenous ligand for the delta 9-tetrahydrocannabinol (delta 9-THC) receptor. The purpose of these studies was to determine whether AN or delta 9-THC can affect the cerebral circulation. With the use of the closed cranial window AN and delta 9-THC (10(-13)-10(-3) M) were topically applied to rabbit cerebral arterioles and effects on diameter were measured with a microscope. AN and delta 9-THC similarly induced a dose-dependent dilation starting at concentrations as low as 10(-12) M. Maximum dilation for AN was 25% and that for delta 9-THC 22%. Topical coapplication of indomethacin, a cyclooxygenase inhibitor, completely blocked dilation, whereas the free radical scavengers superoxide dismutase and catalase or the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) had no effect on AN-induced dilation. The cerebrospinal fluid level of prostaglandin E2 increased only in response to 10(-7) M and greater AN and was not affected by delta 9-THC. [3H]AN superfused through the cranial window was 20% converted to arachidonic acid. These results show that AN and delta 9-THC can modulate cerebral arterioles, likely by stimulating release and metabolism of endogenous arachidonic acid. Whether dilation is due to vasodilator eicosanoids, or other vasoactive agents whose synthesis or release is cyclooxygenase dependent, is uncertain.

Administration, Topical↗
PubMed1986

Pre- and intraoperative localization of small bowel arteriovenous malformation.

Patients with chronic gastrointestinal bleeding with no source found after standard radiographic and endoscopic procedures are diagnostic challenges. Since angiodysplasia is a frequent cause of such bleeding, selective angiography has become an essential diagnostic tool in identifying arteriovenous malformations (AVM) of the large and small bowel. In addition to preoperative identification, some method of intraoperative localization is essential to assure removal of the involved segment. In a patient with a 7-year history of gastrointestinal bleeding from an AVM of the small bowel, a technique of preoperative angiographic catheter placement with intraoperative confirmation of catheter position proved a useful way to find such small bowel lesions and insured adequate but not excessive resection.

Aged↗
PubMed1986

"Composite" tumor--mixed squamous cell and small-cell anaplastic carcinoma of the larynx.

Mixed squamous and oat cell carcinomas (composite neoplasms) of the larynx behave aggressively with a propensity toward early dissemination. Diagnosis may not be made until definitive surgery is performed. The extent of surgery must be determined by the size and site of the primary neoplasm and the physiologic status of the patient. In our experience, surgery has adequately controlled the primary disease. A metastatic work-up is essential. Entry into a comprehensive program employing adjunctive radiotherapy and chemotherapy are strongly recommended. Theories concerning histogenesis remain controversial and include two separate colliding tumors, differentiation from a single cell line, or divergent differentiation of a single cell line.

Carcinoma, Small Cell↗
PubMed1976

The hyperkinetic child syndrome: the need for reassessment.

The dramatic increase in the incidence of hyperkinesis witnessed in recent years constitutes a growing concern for the children so classified. Some relevant issues are discussed in terms of (a) diagnostic practices, (b) treatment practices, and (c) changing views about the nature of the disorder itself. Rather than focusing on the child as a source of the problem (as has typically been the case), future research and practices need to demonstrate a broad-based perspective on the adjustment problems of these children that examines "situational" determinants and institutional policies.

Amygdala↗