PubMed Health⌕ Search

Biomedical subjects

L Bergström

Publications and source records attributed to L Bergström.

9 recordsLinked to original sources
PubMed1991

Regional distribution of somatostatin receptor binding and modulation of adenylyl cyclase activity in Alzheimer's disease brain.

We have previously reported a reduction in the inhibitory effect of somatostatin on adenylyl cyclase activity in the superior temporal cortex of a group of Alzheimer's disease cases, compared to a group of matched controls. In the present study, the levels of high affinity 125I-Tyr11-somatostatin-14 binding, its modulation by guanine nucleotides and the effects of somatostatin on adenylyl cyclase activity have been measured in preparations of frontal cortex, hippocampus, caudate nucleus and cerebellum from the same patient and control groups. A significant reduction in 125I-Tyr11-somatostatin-14 binding was observed in the frontal cortex, but not other regions, of the Alzheimer's disease group, compared with control values. The profiles of inhibition of specific 125I-Tyr11-somatostatin-14 binding by Gpp(NH)p were similar in all regions in both groups. No significant differences in basal, forskolin-stimulated, or somatostatin and neuropeptide Y inhibitions of adenylyl cyclase activity were found between the two groups. The pattern of change of somatostatin binding in the Alzheimer's disease cases observed in the present study differs from the reported pattern of loss of somatostatin neurons and may be secondary to the degeneration of somatostatin receptor-bearing cholinergic afferents arising from the nucleus basalis. The results of this study indicate that impaired somatostatin modulation of adenylyl cyclase is not a global phenomenon in Alzheimer's disease brain and also that there are no major disruptions of somatostatin receptor-G-protein coupling or of adenylyl cyclase catalytic activity in this disorder.

Adenylyl Cyclases↗
PubMed1990

Selective agonists of tachykinin binding sites.

Three types of binding sites for the mammalian tachykinins, ie Substance P (SP) Neurokinin A (NKA) and Neurokinin B (NKB), have been found in both the central and peripheral nervous systems. Substance P binds to the NK-1 subclass of binding site while NKA and NKB are less selective endogenous ligands, which preferentially interact with the NK-2 and NK-3 subclasses of binding sites, respectively. Complementary strategies, including 3-dimensional structure analysis by NMR spectroscopy and structure-activity relationship led to the design of selective agonists of these binding sites. [Pro9] SP, [Pro10] SP and the cyclic analogues [Cys3,6, Tyr8, Pro9] SP and [Cys3,6, Tyr8, Pro10] SP are selective NK-1 agonists. [Lys5] NKA(4-10) is a water soluble NK-2 potent agonist. Finally, [Pro7] NKB, which completely discriminates NK-2 and NK-3 binding sites, is a water-soluble NK-3 selective agonist.

Amino Acid Sequence↗
PubMed1979

Enkephalin levels decrease in rat striatum during morphine abstinence.

Male Sprague-Dawley rats were treated with morphine for 11 days. Saline-injected animals served as controls. The striatal enkephalin levels were measured with a radioimmunoassay 2, 24 and 48 h after withdrawal. There was no change 2 h after the last morphine injection, but a marked reduction after 24 h and a slight decrease after 48 h. No decrease in enkephalin levels was found 12 and 24 h after a single dose of 20 mg/kg morphine.

Animals↗
PubMed1979

The prognosis of near-drowned children.

Thirty children were treated for near-drowning in the Children's Hospital, University of Helsinki during 1971--1976. The patients were divided into 3 groups according to the prognosis: group I included 13 children (43%) with a favourable prognosis, group II four children (13%) with a less favourable prognosis who developed severe sequelae, and group III 13 children with poor prognosis and in whom the subsequent outcome proved fatal. The surviving children underwent neurological, neurophysiological and psychological examination 6--58 months after the accident. The children in group I had slight neurological or psychological signs, some children presented a lowered intellectual functioning level. The children in group II were tetraplegic, unable to speak and had convulsions. The following factors were important in affecting prognosis: the longer the immersion time, the worse the prognosis. However, prognosis could still be favourable with an immersion-time of 11-20 min. Prognosis was bad if the first pH value was less than 7.00. The arterial oxygen pressure values measured during the treatment did not correlate with the prognosis but a low rectal temperature on admission was usually associated with a bad prognosis. The degree of EEG-disturbance had a prognostic value. However, the follow-up recording correlated better with the prognosis than the recordings during the first 24 hours, after which worsening of the EEG sometimes showed a progressive brain lesion.

Adolescent↗
PubMed1977

Cerebrospinal fluid sorbitol and myoinositol in diabetic polyneuropathy.

Changes in cerebrospinal fluid (CSF) concentrations of sorbitol and myoinositol in 21 patients with diabetic polyneuropathy were studied with gas-liquid chromatography. The sorbitol concentration was significantly increased in diabetic patients with elevated plasma glucose. Myoinositol concentration was significantly decreased in patients with polyneuropathy compared with the controls. Both alterations in polyol concentrations of the CSF were present already two months from onset of symptoms of diabetes. Patients with peripheral polyneuropathy receiving oral hypoglycemic drugs did not have elevated plasma glucose and CSF sorbitol levels, but showed significantly decreased CSF myoinositol concentrations compared with the controls. These observations suggest that myoinositol concentration may be decreased in the central nervous system in adult onset mild diabetes with normal plasma glucose and that the decrease in the myoinositol in CSF possibly is connected with the development of neuropathy.

Adult↗
PubMed1975

The transient global amnesia syndrome. An analysis of 35 cases.

On basis of 35 patients who have suffered from transient global amnesia the pathophysiological mechanisms of this syndrome are discussed. Our impression is that the primary cause of this syndrome is a transient ischemia of the hippocampus, an opinion common with most earlier authors. The possibility of a unilateral hippocampal disturbance resulting in transient global amnesia is discussed. We are inclined to regard the local hippocampal ischemia as arising from insufficiency of the anterior chorioidal artery and thus as a sequel of internal carotid insufficiency, which has earlier been proved to result from various rotatory, flexion, and extension movements of the neck.

Adult↗