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Biomedical subjects

L Bergström

Publications and source records attributed to L Bergström.

At least 73 records · Page 4Linked to original sources
PubMed1990

Use of lysimeters to estimate leaching of pesticides in agricultural soils.

In this review of lysimeters, different aspects concerning soil-filling technique, lysimeter size and materials, and drainage-system type are discussed. The placement of lysimeters in the field is dealt with, as are other types of field measurements that can provide complementary information. Evaluations of various properties are based on the assumption that the lysimeters are to be used for estimating pesticide leaching. Guidelines for use in designing a suitable lysimeter experiment for this purpose are described, with special emphasis placed on using the results as a basis for pesticide registration. In this context, some general recommendations are identified. Concerning the lysimeter itself, stress is placed on the importance of using undisturbed soil monoliths. It is recommended that two soil types, i.e. sand and clay, be used and that the management practices carried out closely resemble normal farming practices. Further recommendations include weekly water sampling, two watering regimes, and use of the normal and double the normal application rate of pesticides.

Journal Article↗
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↗
PubMed1987

Interaction of tachykinins with their receptors studied with cyclic analogues of substance P and neurokinin B.

The activities of two groups of cyclic agonists of substance P (SP) have been studied. The disulfide bridge constraints have been designed on the basis of conformational studies on SP and physalaemin indicating an alpha-helical structure for the core of these two tachykinins (group I) and a folding of the C-terminal carboxamide towards the side chains of the glutamines 5 and 6 (group II). Only peptides simulating the alpha-helix present substantial potencies. [Cys3,6]SP is as active as SP in inhibiting 125I-labeled Bolton and Hunter SP-specific binding on rat brain synaptosomes and on dog carotid bioassay, two assays specific for the neurokinin 1 receptor. Moreover, [Cys3,6]SP is as potent as neurokinin B in inhibiting 125I-labeled Bolton and Hunter eledoisin-specific binding on rat cortical synaptosomes as well as in stimulating rat portal vein, two tests specific for the neurokinin 3 receptor. Interestingly, in contrast to neurokinin B, [Cys3,6]SP is a weak agonist of the neurokinin 2 receptor subtype, as evidenced by its binding potency in inhibiting 3H-labeled neurokinin A-specific binding on rat duodenum and in inducing the contractions of the rabbit pulmonary artery, a neurokinin 2-type bioassay. To increase the specificity of the cyclic analogue [Cys3,6]SP positions 8 and 9 were modified. [Cys3,6, Tyr8, Ala9]SP is slightly less selective than SP for the neurokinin 1 receptor subtype. [Cys2,5]neurokinin B constitutes a selective cyclic agonist for the neurokinin 3 receptor. The very weak potencies of the peptides from group II indicate that a certain degree of flexibility in the C-terminal moiety is required. Collectively, these results suggest that the neurokinin 1 and neurokinin 3 tachykinin receptors may recognize a similar three-dimensional structure of the core of the tachykinins. Different orientations of the common C-terminal tripeptide may be related to the selectivity for the different receptor subtypes.

Amino Acid Sequence↗
PubMed1987

[3H]neurokinin B and 125I-Bolton Hunter eledoisin label identical tachykinin binding sites in the rat brain.

[3H]Neurokinin B ([3H]NKB) of high specific activity (75 Ci/mmol) was synthesized for study of its binding to crude synaptosomes from the rat cerebral cortex. The specific binding of [3H]NKB (75% of total binding) was temperature dependent, saturable, and reversible. Scatchard analyses and Hill plots showed the existence of a single population of noninteracting binding sites (KD = 4.3 nM; Bmax = 123 fmol/mg of protein). Competition studies indicated the following rank order of potencies among tachykinins: NKB greater than eledoisin (E) greater than kassinin greater than physalaemin greater than neurokinin A (NKA) greater than substance P (SP), a result suggesting that NKB might be the endogenous ligand for [3H]NKB binding sites. It is of interest that 127I-Bolton Hunter (BH) NKA (127I-BHNKA) was much more potent than NKA in inhibiting the specific binding of [3H]NKB, which raises certain questions concerning the use of 125I-BHNKA as a ligand for NKA binding sites in the brain. These results, as well as those obtained with different SP analogues, show a close similarity to those obtained previously with 125I-BHE binding to cortical synaptosomes. This suggested that the two ligands labeled identical binding sites. In addition, using either [3H]NKB or 125I-BHE as ligands, similar displacement curves were obtained with increasing concentrations of NKB and 127I-BHE. The similarity of the [3H]NKB and 125I-BHE binding sites was further confirmed by comparison of their localization on rat brain sections by autoradiography. The distribution of binding sites for [3H]NKB and 125I-BHE was identical throughout the brain, and the highest density of binding sites for the two ligands was found in layers IV and V of the cerebral cortex, the paraventricular nucleus of the hypothalamus (magnocellular part), and the ventral tegmental area.

Animals↗
PubMed1987

3H-neurokinin A labels a specific tachykinin-binding site in the rat duodenal smooth muscle.

3H-Neurokinin A (3H-NKA) with high specific activity (75 Ci/mmol) was synthesized to study NKA (NK-2)-binding sites on membrane preparations of various tissues in the rat, including brain, spinal cord, duodenum, vas deferens, and ileum. The binding capacity of 3H-NKA (0.9 nM) was very low in membrane preparations of different central nervous system regions and the ileum smooth muscle (0.2-2 fmol/mg of protein). In contrast, relatively high specific binding was found in membrane suspensions of the rat duodenal smooth muscle (18 fmol/mg of protein) and the vas deferens (8 fmol/mg of protein). 3H-NKA-binding sites were further characterized on the rat duodenal smooth muscle. The specific binding of 3H-NKA was shown to be temperature dependent, saturable, reversible, and increased in parallel with the protein concentration. Scatchard analyses and Hill plots of equilibrium binding studies in the concentration range of 0.40-30 nM revealed that 3H-NKA bound to a single class of noninteracting binding sites (Bmax = 270 fmol/mg of protein, KD = 13.3 nM). Displacement of 3H-NKA with different tachykinin-related peptides gave the following rank order of potencies: NKA greater than NKA (4-10) greater than kassinin greater than eledoisin greater than NKB much greater than substance P greater than physalaemin, which suggests that the binding site labeled by 3H-NKA is different from substance P (NK-1)-and NKB (NK-3)-binding sites. The biological activities of tachykinins and related peptides were tested by measuring their contractile effects on the rat duodenum and rabbit pulmonary artery, two tissues known to be sensitive for NKA. Ki values were correlated with the EC50 obtained in biological assays. The results revealed a significant correlation (r = 0.86, p less than 0.01) between Ki and EC50 values obtained in the isolated rabbit pulmonary artery, whereas there was no significant correlation between binding affinities and biological responses on the rat duodenum (r = 0.62, p greater than 0.05).

Animals↗
PubMed1986

A cyclic analogue selective for the NKB specific binding site on rat brain synaptosomes.

The cyclic analogue of NKB, [Cys2,Cys5]NKB is as active as SP and NKB in the guinea-pig ileum bioassay. Furthermore, [Cys2,Cys5]NKB is a selective substrate for the [3H]NKB specific binding site on rat cortical synaptosomes. Its binding potencies for [3H]NKB and 125I-BHSP binding sites, IC50 = 5.2 nM and 3.4 microM respectively were close to those observed for NKB.

Animals↗
PubMed1986

Substance P receptors in primary cultures of cortical astrocytes from the mouse.

Binding sites for substance P were labeled on intact cortical glial cells from newborn mice in primary culture using 125I-labeled Bolton-Hunter-labeled substance P. Maximal specific binding (95% of total binding) was reached after 2-3 weeks in culture. The binding was saturable, reversible, and temperature dependent. Scatchard and Hill analysis revealed a single population of noninteracting high-affinity binding sites (Kd, 0.33 nM; Bmax, 14.4 fmol per dish). Competition studies made with tachykinins and substance P analogues indicated that the characteristics of the 125I-labeled Bolton-Hunter labeled substance P binding sites on glial cells were identical to those on rat brain synaptosomes. 125I-labeled Bolton-Hunter labeled substance P binding sites were visualized by autoradiography, and differences in the intensity of labeling were seen among astrocytes. Substance P was found to stimulate phosphatidylinositol turnover; the EC50 value (0.36 nM) was identical to the IC50 value (0.38 nM) determined in binding studies. 125I-labeled Bolton-Hunter labeled substance P binding sites were also found on astrocytes derived from other brain structures and from the spinal cord of mice.

Animals↗
PubMed1985

Morbid obesity, gastric plication and a severe neurological deficit.

A 39-year-old man had protracted vomiting after gastric plication for morbid obesity. Within three months he lost 53 kg in weight and developed neuromuscular weakness, especially in the lower extremities. Clinical and laboratory studies suggested both radicular and peripheral neuropathy. One year later the condition was only marginally improved: he took only few steps unsupported. The apparent etiology is malnutrition but the primary cause remained unknown.

Adult↗
PubMed1985

Memory and psychomotor impairment following high-dose interferon treatment in amyotrophic lateral sclerosis.

Patients with amyotrophic lateral sclerosis were treated with high-dose intravenous infusion of human leukocyte interferon for six days. Neuropsychological examinations were carried out before, during and after the treatment. Marked reversible dysfunction was detected in immediate memory functions, coordination of hand movements, and drawing. Motor perseveration, micrographia, and slowing of behaviour were also observed. Changes appeared four to 12 days after start of treatment, with the peak on days six to eight. Recovery was almost complete by day 15. Intellectual ability, as measured by three WAIS subtests, praxis of hand movements, visuognostic functions, speech, reading, writing, and calculation remained essentially unaffected. The profile of the neuropsychological deficits observed, the absence of defects typical of focal posterior cortical lesions, the simultaneously slowed electroencephalographic activity with frontal accentuation, and the increased central conduction times of brain stem auditory evoked potentials suggest frontobasal involvement.

Aged↗