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Biomedical subjects

E Shohami

Publications and source records attributed to E Shohami.

134 records · Page 8Linked to original sources
PubMedDate not supplied

The effects of the acetylcholinesterase inhibitor ENA713 and the M1 agonist AF150(S) on apolipoprotein E deficient mice.

Apolipoprotein E (apoE)-deficient and control mice were treated chronically with either the acetylcholinesterase (AChE) inhibitor ENA713, or the M1 muscarinic agonist AF150(S). Both treatments reversed the spatial working memory impairment of apoE-deficient mice but they differed in their effects on the levels of brain AChE activity. AF150(S) enhanced the brain AChE activity of apoE-deficient mice and rendered it similar to that of the untreated controls, whereas ENA713 reduced the brain AChE activity of control mice but had no effect on that of apoE-deficient mice. These findings suggest that AChE inhibition and M1 muscarinic activation have similar beneficial cognitive effects on apoE-deficient mice, but that the cellular and molecular mechanisms underlying these effects differ.

Animals↗
PubMedDate not supplied

The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain.

Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB2, on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 +/- 3.5 min. in the control rats. The rats which received indomethacin recovered faster (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Postischemic production of eicosanoids in gerbil brain.

The postischemic production of PGE2, PGD2, 6-keto-PGF1 alpha, and TXB2 in brain tissue was studied in Mongolian gerbils using tissue extraction as well as a new ex vivo method. This new method permits the study of prostaglandin synthesis in slices from discrete areas of the brain (cortex, hippocampus, striatum, hypothalamus). Gerbils were sacrificed at 0, 5, and 30 minutes, and 4 and 24 hours after a 15-minute occlusion of both carotid arteries. Apart from 6-keto-PGF1 alpha, tissue prostaglandins determined by the extraction method were significantly increased 3 and 30 minutes after reperfusion. The most pronounced changes found by the ex vivo method were increased productions of PGD2 immediately after reperfusion (285% in cortex, 215% in hypothalamus) and PGE2 (350% in hippocampus, 320% in striatum) 4 hours after reperfusion. At 24 hours after reperfusion PGE2 and PGD2 synthesis were significantly decreased by 23-70% of the values obtained from sham-operated controls. Thromboxane increased slightly in all areas after recirculation and subsequently decreased to values below the control level in striatum. The results obtained by ex vivo incubation of tissue slices demonstrate that ischemia and subsequent recirculation cause site-, time-, and PG-specific changes of tissue eicosanoid production.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Deteriorating stroke model: histopathology, edema, and eicosanoid changes following spinal cord ischemia in rabbits.

Secondary motor dysfunction is often observed following ischemic episodes in the central nervous system. To study potential mechanisms of postischemic motor deterioration, we developed a rabbit spinal cord ischemia model that has characteristics similar to the clinical condition termed deteriorating stroke. In this model, 70% of the rabbits regained substantial motor function by 4 hours after complete hindlimb paralysis during lumbar spinal cord ischemia; however, over the next 20 hours motor function steadily declined to the point where only 30% of the rabbits had minimal hopping function. The role of eicosanoids in spinal cord ischemia was studied by radioimmunoassay of several prostaglandins (6-keto-PGF1 alpha, PGE2, and TxB2) in the spinal cord. After 5 minutes of reperfusion, TxB2 levels were markedly elevated (p less than 0.05) while 6-keto-PGF1 alpha levels did not change. The TxB2:6-keto-PGF1 alpha ratio was also significantly increased. After 30 minutes of reperfusion, PGE2 levels were also elevated (p less than 0.05). Tissue edema measured by microgravimetry was also increased after 30 minutes of reperfusion in both gray and white matter. By 4 hours of reperfusion, rabbits regained near-normal hindlimb motor function while PGE2, 6-keto-PGF1 alpha, TxB2, and tissue water content were back to normal. However, by 18 hours of reperfusion, when hindlimb function was deteriorating, TxB2 levels were elevated again, and edema in gray and white matter was increased as was the number of necrotic neurons observed by light microscopy. These results suggest that the secondary deterioration of motor neurologic function was due to the excess formation of TxA2 primarily in the late reperfusion phase. However, further studies are necessary to elucidate the relation of TxA2 with ischemic neural injury.

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PubMedDate not supplied

Superoxide dismutase activity is not affected by closed head injury in rats.

Superoxide anion radicals are generated in association with prostaglandin production, and are implied in the mediation of secondary brain damage following cerebral ischemia or injury. In a model of closed head injury in rats we have demonstrated the activation of phospholipase A2 (PLA2) and the increased production of eicosanoids in the post-trauma period. In the present study we investigated the role of superoxide dismutase (SOD) in this model. Head trauma was induced over the left cerebral hemisphere of ether anesthetized rats by a calibrated weight drop device. Cortical tissue samples were taken 15 min, 4 and 24 h later. SOD activity was assayed by its ability to inhibit the xanthine oxidase-cytochrome c reduction. There was no significant change in SOD activity in any of the regions studied - the site of injury, and contralateral region as well as the remote frontal lobes of both hemispheres. Although intense PLA2 activity and production of eicosanoids was previously found in some of these regions, activity of SOD was unaffected. These results do not support an important role for endogenous SOD up to 24 h after head injury.

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PubMedDate not supplied

The mixed lipoxygenase/cyclooxygenase inhibitor SK&F 105809 reduces cerebral edema after closed head injury in rat.

Closed head injury in rats induces edema formation, which is indicated by a decrease in cerebral specific gravity and an increase in water content. We previously described the activation of the eicosanoid metabolic cascade, namely, activation of PLA2 and accumulation of products of both 5-lipoxygenase (5-LO) and cyclo-oxygenase (CO) in the same model of head injury. The present study was designed to determine the effect of a novel drug, SK&F 105809, a dual inhibitor of 5-LO and CO on cerebral edema formation after head injury in rats. Rats, under ether anesthesia, were subjected to sham operation or trauma induced by weight-drop device impacting over the left calvarium. One group of traumatized rats received 0.9% saline and served as control and two other groups were treated with SK&F 105809, 20 or 30 mg/kg, i.p. immediately after the impact. In one group treatment was repeated additionally 2.5 h post-trauma. Four hours after trauma, rats were sacrificed and brain edema was evaluated. SK&F 105809 treated rats which received 30 mg/kg had significantly less brain edema, as measured by both gravimetry and water content, at 4 h after trauma. The lower dose, 20 mg/kg, had no effect. Our results suggest that treatment with a mixed 5-LO/CO inhibitor shortly after head injury will result in less brain edema and ultimately improved functional outcome.

Animals↗
PubMedDate not supplied

Communication strategies used during pediatric dental treatment: a pilot study.

PURPOSE: Effective verbal communication is essential for successful dental treatment. The purpose of this study was to qualitatively and quantitatively examine communication techniques used by pediatric postdoctoral students during treatment. The operation of a communication model comprised of three linguistic approaches-permissive, empathic and personal-together with other strategies common to all three, was examined. METHODS: The study group consisted of 24 children (14 boys and 10 girls), 3 to 12 years of age. All four dentists were 2nd year residents in pediatric dentistry. Conversations were taped and analyzed linguistically and statistically. The frequency of use of each approach was tabulated and correlated to the children's reported anxiety, cooperation during treatment, success of treatment, and mood at the end of treatment. RESULTS: All dentists used the three approaches; the permissive approach, which supplied procedural information, was the most frequently used approach. The empathic approach was the least frequently used. Correlation tests showed that the empathic approach was most significantly related to the success of the treatment. Components of the permissive approach that contributed to the success of treatment were sensory information and supplying reasons. CONCLUSIONS: Although generalization is limited because of the small sample, improving verbal conversational skills, emphasizing certain strategies, and improving linguistic abilities will contribute to better communication between child and pediatric dentist and to better cooperation and success in treatment.

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