Biomedical subjects

J Miesner

Publications and source records attributed to J Miesner.

4 recordsLinked to original sources

PubMed2005

Zinc and lead poisoning in wild birds in the tri-state mining district (Oklahoma, Kansas, and Missouri).

The Tri-State Mining District (Oklahoma, Kansas, and Missouri) is contaminated with Pb, Cd, and Zn from mining, milling and smelting. Metals have been dispersed heterogeneously throughout the District in the form of milled mine waste ("chat"), as flotation tailings and from smelters as aerial deposition or slag. This study was conducted to determine if the habitat has been contaminated to the extent that the assessment populations of wild birds are exposed to toxic concentrations of metals. American robins (Turdus migratorius), northern cardinals (Cardinalis cardinalis), and waterfowl had increased Pb tissue concentrations (p < 0.05) compared with Pb tissue concentrations from reference birds, and the exposure of songbirds to Pb was comparable with that of birds observed at other sites severely contaminated with Pb. Mean activities of the Pb-sensitive enzyme delta-aminolevulinic acid dehydratase (ALAD) were decreased by >50% in red blood cells in these birds (p < 0.05). Several birds had tissue concentrations of Pb that have been associated with impaired biological functions and external signs of poisoning. Cadmium was increased in kidneys of songbirds (p < 0.05), but no proximal tubule cell necrosis associated with Cd poisoning was observed. Zinc concentrations in liver and kidney of waterfowl were significantly higher (p < 0.05) than reference values. The increased environmental concentrations of Zn associated with mining in the District accounted for the pancreatitis previously observed in five waterfowl from the District. The District is the first site at which free-flying wild birds have been found to be suffering severe effects of Zn poisoning.

Animals↗

PubMed2003

Eye movement abnormalities in essential tremor may indicate cerebellar dysfunction.

Experimental and clinical data indicate that the cerebellum is involved in the pathophysiology of advanced stages of essential tremor (ET). The aim of this study was to determine whether a dysfunction also affects cerebellar structures involved in eye movement control. Eye movements of 14 patients with ET and 11 age-matched control subjects were recorded using the scleral search-coil technique. Vestibular function was assessed by electro-oculography. Eight ET patients had clinical evidence of intention tremor (ET(IT)); six had a predominantly postural tremor (ET(PT)) without intention tremor. ET patients showed two major deficits that may indicate cerebellar dysfunction: (i) an impaired smooth pursuit initiation; and (ii) pathological suppression of the vestibulo-ocular reflex (VOR) time constant by head tilts ('otolith dumping'). In the step ramp smooth pursuit paradigm, the initial eye acceleration in the first 60 ms of pursuit generation was significantly reduced in ET patients, particularly in ET(IT) patients, by approximately 44% (mean 23.4 degrees/s(2)) compared with that of control subjects (mean 41.3 degrees/s(2)). Subsequent steady-state pursuit velocity and sinusoidal pursuit gain (e.g. 0.4 Hz: 0.90 versus 0.78) were also significantly decreased in ET patients, whereas pursuit latency was unaffected. The intention tremor score correlated with the pursuit deficit, e.g. ET(IT) patients were significantly more affected than ET(PT) patients. Gain and time constant (tau) of horizontal VOR were normal, but suppression of the VOR time constant by head tilt ('otolith dumping') was pathological in 41% of ET patients, particularly in ET(IT) patients. Saccades and gaze-holding function were not impaired. The deficit of pursuit initiation, its correlation with the intensity of intention tremor, and the pathological VOR dumping provide additional evidence of a cerebellar dysfunction in the advanced stage of ET, when intention tremor becomes part of the clinical symptoms, and point to a common pathomechanism. The oculomotor deficits may indicate an impairment of the caudal vermis in ET.

Adult↗

PubMed1993

Postpyloric stimuli are necessary for the normal control of meal size in real feeding and sham feeding rats.

When 0.8 M sucrose is sham fed, intake increases progressively on consecutive tests and then plateaus. Interspersing two real feeding tests between sham feeding tests prevents this increase in sham intake [J. D. Davis and G. P. Smith. Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R1228-R1235, 1990]. This is consistent with an acquired control of ingestion based on an association between an oropharyngeal conditioned stimulus (CS) and a postingestional unconditioned stimulus (UCS). To determine if this postingestional UCS has a gastric or postgastric origin (or a combined one), we confined ingested 0.8 M sucrose to the stomach on real feeding and sham feeding tests by closing the pylorus with an inflatable Silastic cuff. Rats were tested on seven sham feeding tests separated by two real feeding tests and then on six consecutive sham feeding tests. In contrast to our previous results [Davis and Smith. Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R1228-R1235, 1990], intake increased progressively on the real feeding and both types of sham feeding tests. We conclude that both gastric and postgastric stimuli act as a UCS for the acquired control of meal size.

Animals↗

PubMed1992

Intravenous infusion of CCKA-receptor antagonist increases food intake in rats.

To test the hypothesis that endogenous cholecystokinin (CCK) released from the small intestine by ingested food produces a satiating effect by acting at CCKA-receptors, we measured the effect of slow continuous intravenous infusions of three doses of MK-329, a potent and selective CCKA-antagonist, on food intake during 2.5-h tests in 13 Sprague-Dawley male rats after 1 h of food deprivation. MK-329 increased food intake significantly and the lowest dose tested (0.5 mg.kg-1.h-1) produced the most consistent effect on cumulative intake. Part of the increased food intake under these conditions was due to a decrease in the satiating effect of food ingested at the first meal on the postprandial intermeal interval. These results are consistent with, but do not prove, the hypothesis that the satiating effect of endogenous CCK released from the small intestine by ingested food is mediated by CCKA-receptors.

Animals↗