Search PubMed⌕ Search

Biomedical subjects

M Davis

Publications and source records attributed to M Davis.

At least 433 records · Page 24Linked to original sources

Boron-11 MRI and MRS of intact animals infused with a boron neutron capture agent.

Boron neutron capture therapy (BNCT) depends on the delivery of boron-containing drugs to a targeted lesion. Currently, the verification and quantification of in vivo boron content is a difficult problem. Boron-11 spectroscopy was utilized to confirm the presence of a dimeric sulfhydryl dodecaborane BNCT agent contained in an intact animal. Spectroscopy experiments revealed that the decay time of transverse magnetization of the boron-11 spins was less than 1 ms which precluded the use of a 2DFT imaging protocol. A back-projection protocol was developed and utilized to generate the first boron-11 image of a BNCT agent in the liver of an intact Fisher 344 rat.

Animals↗

Apomorphine, d-amphetamine, strychnine and yohimbine do not alter prepulse inhibition of the acoustic startle reflex.

Rats were presented with noise bursts alone or noise bursts 60 ms after presentation of either a 60 dB or an 80 dB prepulse after injection of the dopamine agonists apomorphine (3 mg/kg) or d-amphetamine (4 mg/kg), the glycine antagonist strychnine (1.5 mg/kg) or the alpha 2 antagonist yohimbine (5 mg/kg). Presentation of prepulses inhibited startle, with greater inhibition following an 80 dB versus 60 dB prepulse. Apomorphine, d-amphetamine and strychnine increased overall startle levels but did not attenuate prepulse inhibition, since the absolute change in startle following prepulse presentation was significantly greater after administration of these drugs. A lower dose of apomorphine also increased startle but had no effect on prepulse inhibition using test intervals of 10, 60, 100, 200 or 1000 ms. While these drugs did decrease per cent prepulse inhibition, this seemed wholly attributable to their increasing overall startle levels, rather than a real attenuation of prepulse inhibition. Yohimbine did not alter either startle baseline or prepulse inhibition. The results do not support the conclusion that overactivity of dopamine systems attenuates prepulse inhibition and, in addition, suggest that prepulse inhibition does not result from activation of either glycine or norepinephrine projecting to alpha 2 adrenergic receptors.

Acoustic Stimulation↗

Anxiolytic effects of buspirone and gepirone in the fear-potentiated startle paradigm.

Fear potentiation of the acoustic startle reflex was produced by eliciting startle responses in the presence of a light that had been previously paired with a shock. Buspirone (0.6-5.0 mg/kg) and gepirone (1.25-10.0 mg/kg), but not their common metabolite, 1-PP (0.5-40 mg/kg), produced a dose-dependent reduction of fear-potentiated startle. These doses of buspirone and gepirone slightly increased baseline startle levels. Reduction of fear-potentiated startle appears to involve supraspinal sites of action, since intraventricular but not intrathecal administration of buspirone (200 micrograms) reduced fear-enhanced startle. Both buspirone and gepirone were highly efficacious in this model compared to other animal tests that are used to study anxiolytic compounds.

Animals↗

Serotonin does not mediate anxiolytic effects of buspirone in the fear-potentiated startle paradigm: comparison with 8-OH-DPAT and ipsapirone.

The present study evaluated the role of various neurotransmitter systems in mediating buspirone's blockade of the fear-potentiated startle effect, where acoustic startle amplitude is normally increase in the presence of a light previously paired with a shock. Large lesions of the dorsal and median raphe nuclei or IP injections of the serotonin antagonists cinanserin (10 mg/kg) or cyproheptadine (5 mg/kg) did not alter fear-potentiated startle, nor did these treatments prevent buspirone (5 or 10 mg/kg SC) from blocking fear-potentiated startle. The 5-HT 1A agonist 8-OH-DPAT (2.5-10.0) did not block fear-potentiated startle even at doses that produced a marked "5-HT syndrome". Another 5-HT 1A agonist, ipsapirone (10-20 mg/kg), blocked potentiated startle only at a very high dose (40 mg/kg). p-Chlorophenylalanine and p-chloroamphetamine did not alter fear-potentiated startle. Finally, pretreatment with the benzodiazepine receptor antagonist RO-15-1788 (1 mg/kg); the opiate antagonist naloxone (2 mg/kg) or the alpha 2-adrenergic antagonist yohimbine (5 mg/kg) did not reduce fear-potentiated startle, nor did they prevent buspirone from blocking fear-potentiated startle. Taken together, the data do not support the hypothesis that buspirone's anxiolytic effects are mediated by actions at 5-HT 1A receptors and more generally indicate that serotonergic neurons do not play an important role in fear-potentiated startle.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Intramural hemorrhage simulating gastric neoplasm.

We report a case of benign gastric ulcer with secondary extensive intramural hemorrhage causing a radiographic appearance consistent with a large ulcerated gastric neoplasm. This is the second such case reported and the first studied with sonography and computed tomographic scan. A brief review of the literature on intramural gastric hematoma is presented.

Adult↗

Small bowel edema: mosaic pattern.

We report an unusual radiographic appearance of small bowel submucosal edema produced by obstruction from metastatic colorectal carcinoma. The distinctive muscosal pattern of raised polygonal plaques is the same mosaic pattern described in the colon and referred to as "urticaria." This mosaic pattern in the small bowel has not previously been reported.

Aged↗

Intussusception secondary to squamous carcinoma of the lung.

This report describes unusual radiologic and pathologic findings in a patient with multiple small bowel metastases from squamous cell carcinoma of the lung. The diagnostic work-up revealed a large, pleural-based, right lung mass, a large left adrenal mass, two ulcerated small bowel masses, and a unique giant peduncular mass that caused intermittent intussusception. A pertinent review of the literature is presented.

Carcinoma, Squamous Cell↗

Obstructive jaundice from open vessel clip.

Obstructive jaundice occurred 3 years after cholecystectomy in a 49-year-old man. At surgery a large stone was discovered in the common bile duct. Pathologic examination showed that the stone had formed around an open vessel clip. Migration of an open vessel clip to the biliary system with subsequent stone formation has not been reported previously.

Cholestasis↗

Temporal characteristics of enhancement of startle by stimulation of the amygdala.

A previous study demonstrated that electrical stimulation of the amygdala facilitated the acoustic startle reflex. The purpose of the present study was to determine the temporal relationship between activation of the amygdala and its enhancement of the acoustic startle reflex. A single 0.1 msec pulse was delivered to the central nucleus of the amygdala at various times before or after the onset of 20 msec noise burst or a 0.1 msec click. Startle was enhanced when the stimulation occurred within 5 msec of the startle stimulus onset. Electromyographic recordings from the neck muscles demonstrated that the short 6 msec latency startle response was facilitated even when amygdala stimulation was presented 1.25 msec after the onset of the startle stimulus. This indicates that the time for the effects of amygdala stimulation to reach the brain stem startle circuit is less than 5 msec, suggesting a very direct pathway from the amygdala to the startle circuit. The similarity of this effect to fear-potentiated startle is also discussed.

Acoustic Stimulation↗

Enhancement of acoustic startle by electrical stimulation of the amygdala.

The present study demonstrated that electrical stimulation of the amygdala enhanced the acoustic startle response. A 25-ms train of 0.1-ms pulses initiated 5 ms before the onset of a 20-ms noise burst significantly increased startle at currents from 40 to 400 microA. Electrode placements just medial to the amygdala (in the pathway connecting the amygdala to the brain stem) increased startle with the lowest currents. Startle was also increased in all animals with stimulation in the central, medial, and intercalated nuclei of the amygdala. Stimulation in areas surrounding the amygdaloid complex was ineffective. In a second experiment, paired pulses with interpulse intervals between 0.1 and 20.0 ms delivered to the amygdala demonstrated that the stimulated axons had a distribution of refractory periods between 0.6 and 1.0 ms. This suggests that the population of neurons which subserves the enhancement of acoustic startle is fairly homogeneous and has small, myelinated axons.

Acoustic Stimulation↗

Horse pill ("bute") hemorrhage.

Phenylbutazone (PBZ) is a nonsteroidal antiinflammatory drug (NSAID) that is not commonly prescribed due to the high incidence of serious adverse reactions. However, it is still used extensively in equine medicine, and is readily available to those employed in the care and management of horses. Such persons may take the drug indiscriminately, without medical supervision. We present a 33-year-old male race horse track worker who took phenylbutazone horse pills for a chronic toothache and subsequently suffered a major hemorrhage from a gastric ulcer. Human use of phenylbutazone horse pills should be considered by physicians confronted with patients who have upper gastrointestinal symptoms and gastric injury and who belong to this select group.

Adult↗

The assignment of the human gene coding for complement C5 to chromosome 9q22-9q33.

The presence or absence of the human gene for the fifth component of complement (C5) was analysed in 19 human-rodent hybrid cell lines by hybridization to a radiolabelled probe derived from a human C5 cDNA clone. The segregation of C5 in these hybrids suggested that the gene is localized on chromosome 9, in the region 9q21-9qter. In situ hybridization refined the assignment of C5 to chromosome 9q22-33.

Animals↗

Effects of neuropeptide Y on the isolated rabbit iris dilator muscle.

The effects of neuropeptide Y (NPY) were studied on an in vitro preparation of rabbit iris dilator muscle. NPY by itself (10(-11) M to 10(-6) M) had no effect on the resting tension or on the maximal electrically-induced response (MER) of the dilator. Phenylephrine (10(-9) M to 10(-4) M) caused a dose-dependent contraction of the dilator muscle (7.8% to 40.6% of the MER). The addition of NPY 10(-6) M enhanced the phenylephrine-induced muscle contraction (8.8% to 76.8% of the MER) without altering the EC50 value (5 X 10(-6) M) of the phenylephrine dose-response curve. These findings support a modulatory role for NPY on the iris dilator muscle.

Animals↗