Efficacy of disodium 4-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059), a free radical trapping agent, in a rat model of hemorrhagic stroke.

Because free radical mechanisms may contribute to brain injury in hemorrhagic stroke, the effect of the free radical trapping agent disodium 4-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) was investigated on outcome following intracerebral hemorrhage (ICH) in rat. ICH was induced in 20 adult rats by infusion of collagenase into the caudate-putamen. Thirty minutes later rats were treated with NXY-059 (50 mg/kg subcutaneous plus 8.

Effect of FK-506 on inflammation and behavioral outcome following intracerebral hemorrhage in rat.

Beginning 15 min after induction of intracerebral hemorrhage (ICH) by intrastriatal administration of collagenase, rats were treated intramuscularly with FK-506 (3 mg/kg) or with vehicle. Treatment was repeated daily for 7 days. MR imaging 1, 7, and 28 days post-ICH showed that treatment did not affect hematoma size or its subsequent resolution.

Prolonged but delayed postischemic hypothermia: a long-term outcome study in the rat middle cerebral artery occlusion model.

Delayed but prolonged hypothermia persistently decreases cell death and functional deficits after global cerebral ischemia in rodents. Postischemic hypothermia also reduces infarction after middle cerebral artery occlusion (MCAO) in rat. Because initial neuroprotection is sometimes transient and may not subserve functional recovery, especially on demanding tasks, the authors examined whether postischemic cooling would persistently reduce infarction and forelimb reaching deficits after MCAO.

Persistent neuroprotection with prolonged postischemic hypothermia in adult rats subjected to transient middle cerebral artery occlusion.

Postischemic hypothermia provides long-lasting neuroprotection against global cerebral ischemia in adult rats and gerbils. Studies indicate that hypothermia must be prolonged (e.g.

Long-term functional end points following middle cerebral artery occlusion in the rat.

The purpose of the present study was to assess the magnitude and stability of a number of functional deficits in rats subjected to occlusion of the middle cerebral artery (MCAO). Three groups of rats, treated with 90-min, 120-min, or sham occlusion were used in functional studies for 22 weeks following surgery. The following tests were used: methamphetamine-induced rotation, the staircase test, acquisition of operant responding, running-wheel behavior, and performance of operant differential reinforcement of a low-rate responding (DRL) schedule of reinforcement.

Temperature modulation (hypothermic and hyperthermic conditions) and its influence on histological and behavioral outcomes following cerebral ischemia.

Core temperature (T(C)) is a critical determinant of the severity of neural damage that results from focal or global ischemia. Former studies indicated that especially intra-ischemic but also post ischemic mild hypothermia significantly decreased necrotic neural damage of a focal or global insult, as assessed between 3-7 days post-insult. More recent work shows that prolonged post-ischemic hypothermia reduces neural damage and inhibits associated behavioral deficits for up to one year after the insult (i.

Acrylonitrile induces autolysis Bacillus subtilis.

Acrylonitrile (AN) is an industrial chemical used in the manufacture of plastics and other polymers. AN has been reported to be an acute toxin and is a known carcinogen in rodents. When AN was mixed with suspensions of Bacillus subtilis, the bacteria began autolysis.

Ischemic preconditioning in 18- to 20-month-old gerbils: long-term survival with functional outcome measures.

Background And Purpose: In young animals, ischemic preconditioning protects CA1 hippocampal neurons against global ischemia. However, cerebral ischemia occurs most frequently in individuals aged >/=65 years. This study examined the protection provided by ischemic preconditioning in a population of aged (18- to 20-month-old) gerbils.

Diazepam-induced neuroprotection: dissociating the effects of hypothermia following global ischemia.

Global cerebral ischemia produces hippocampal CA1 neuronal loss which in turn leads to deficits in memory related tasks. Previous studies have shown that the benzodiazepine diazepam is effective at attenuating this cell death and the related behavioural impairments. However these studies have been confounded by diazepam-induced hypothermia.

First paleoparasitological analysis of a midden in the Aleutian Islands (Alaska): results and limits.

Excavations on Buldir Island, Aleutian Islands, Alaska, have revealed the remains of several features dated between the 13th and 17th centuries A.D. Soil from an open-air workshop, represented by 2 excavated pits, and a structure built of whale bones were sampled for evidence of parasites and microfloristic remains.

Temporal profile of magnetic resonance imaging changes following forebrain ischemia in the gerbil.

Quantitative T2 magnetic resonance (MR) imaging was used to examine gerbil brains 1, 3, 10, and 30 days after 5 min forebrain ischemia. T2 was increased in the dorsal-lateral striatum 1 and 3 days post-ischemia, and in the hippocampus 3 days post-ischemia. T2 was normal 10 days post-ischemia, and decreased in the hippocampus and dorsal-lateral striatum 30 days post-ischemia.

Competing processes of cell death and recovery of function following ischemic preconditioning.

The goal of the present study was to determine the neuroprotective efficacy of ischemic preconditioning using behavioral, electrophysiological and histological endpoints at various time points up to 90 days postischemia. Gerbils were exposed to a brief, non-injurious episode of forebrain ischemia (1.5 min) on each of 2 consecutive days.

The problem of assessing effective neuroprotection in experimental cerebral ischemia.

In animal models of global and focal ischemia neuroprotection is typically determined by quantifying the degree of cell loss or reduction in infarct volume shortly after the ischemic insult. These methods are unable to reliably detect more subtle forms of neuronal death and dysfunction that arise from injury to non-homogeneous cell populations (e.g.

-(S)-Alpha-phenyl-2-pyridine-ethanamine Dihydrochloride-, a low affinity uncompetitive N-methyl-D-aspartic acid antagonist, is effective in rodent models of global and focal ischemia.

[(S)-Alpha-phenyl-2-pyridine-ethanamine dihydrochloride] (ARL 15896AR) is a low affinity uncompetitive N-methyl-D-aspartic acid receptor antagonist that was tested in animal models of anoxia and ischemia. Pretreatment of rodents with ARL 15896AR extended survival time during exposure to hypoxia. With the rat four-vessel occlusion model of global ischemia (20 min), oral dosing commencing at reflow, resulted in significant protection of the CA1 hippocampal neurons.

Hypothermic neuroprotection. A global ischemia study using 18- to 20-month-old gerbils.

Background And Purpose: Previous studies from this laboratory have shown that mild intraischemic or prolonged (i.e., 12 to 24 hours) postischemic hypothermia conveys long-lasting (1 to 6 months) protection against CA1 injury.

Ischemic preconditioning: a long term survival study using behavioural and histological endpoints.

In this study we sought to determine if ischemic preconditioning provided long term behavioral and histological protection. A second goal was to see if ischemic preconditioning conveys its protective effect on CA1 neurons by altering post-ischemic brain temperature. While preconditioning episodes of short duration ischemia (i.

Postischemic hypothermia. A critical appraisal with implications for clinical treatment.

The use of hypothermia to mitigate cerebral ischemic injury is not new. From early studies, it has been clear that cooling is remarkably neuroprotective when applied during global or focal ischemia. In contrast, the value of postischemic cooling is typically viewed with skepticism because of early clinical difficulties and conflicting animal data.

Congenital clubfoot. Month of conception.

The medical records of 330 children who were born with uncomplicated congenital clubfoot were reviewed retrospectively. To determine their months of conception, the duration of gestation was extrapolated and those which were less than 40 weeks were noted. The years of conception for the studied children were from 1956 to 1994.

Dose dependence of covalent binding of acrylonitrile to tissue protein and globin in rats.

The dose dependence of acrylonitrile (AN) covalent binding to tissue protein, following a single acute exposure over a 100-fold range in dose, was measured. Covalent binding was a linear function of AN dose in the lower dose range (0.02-0.

Biological markers of acute acrylonitrile intoxication in rats as a function of dose and time.

Three markers of acute acrylonitrile (AN) intoxication, namely, tissue glutathione (GSH), tissue cyanide (CN), and covalent binding to tissue protein, were studied as a function of dose and time. Doses administered and responses expected were 20 mg/kg (LD0), 50 mg/kg (LD10), 80 mg/kg (LD50), and 115 mg/kg (LD90). Liver GSH was the most sensitive marker of AN exposure.

Neuroprotection after several days of mild, drug-induced hypothermia.

Stroke trials are initiated after demonstrated pharmacological protection in animal models. NBQX protects CA1 neurons against global ischemia; however, this glutamate antagonist induces a period of subnormal temperature (e.g.

Delayed postischemic hypothermia: a six month survival study using behavioral and histological assessments of neuroprotection.

In the gerbil, brief global forebrain ischemia induces profound habituation and working memory impairments that stem from delayed hippocampal CA1 death. Short duration postischemic hypothermia has been shown to reduce CA1 loss, but such reports are controversial, as it is thought that protection may be transient. The purpose of this study was to investigate whether prolonged postischemic hypothermia provided long-term CA1 and functional neuroprotection.

Synthesis and antifungal activity of C-16 oximino and vinyl amphotericin B derivatives.

Several new C-16 oximino and vinyl derivatives of amphotericin B are described. They are prepared by the reaction of a suitably protected amphotericin B C-16 aldehyde with hydroxylamine derivatives and Wittig reagents, respectively, followed by sequential removal of the protecting groups. The compounds possess potent antifungal activity in vitro, similar to or in some cases superior to that of amphotericin B itself.

Direct measurement of brain temperature during and after intraischemic hypothermia: correlation with behavioral, physiological, and histological endpoints.

The aim of the present study was to evaluate critically the protection afforded by hypothermia against ischemic injury to the hippocampus. Hypothermic treatment was applied selectively to the brain during a 5 min carotid artery occlusion in gerbils. Following a period of recovery, two independent measures were used to assess hippocampal function: (1) an open field test of spatial memory (assessment was made during the first 10 d after ischemia) and (2) measurement of evoked potentials from area CA1 in hippocampal slices (3 weeks after the ischemic episode).