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L Olsson

Publications and source records attributed to L Olsson.

At least 55 records · Page 3Linked to original sources
PubMed1997

A model for quality assessment in primary health care using the tracer condition technique with insulin treated diabetes as one of the tracers.

OBJECTIVE: To find a method for quality assessment in primary health care and to apply this method on a defined disease. DESIGN: General practitioners and hospital doctors worked out a programme for evaluating the quality of outpatient care of patients with insulin treated diabetes as one of five tracers. An expert committee comprising experienced general practitioners and hospital doctors compared two health centres with one outpatient medical department. Data were collected during a defined period combined with a one-year retrospective view, official statistics on medical care, and a questionnaire completed by the patients. SETTING: Two primary health care centres and one outpatient medical department in southwestern Sweden. PATIENTS: 243 insulin treated diabetic patients attending the hospital and 87 insulin treated patients attending the health centres. MAIN RESULTS: There were no difficulties for the expert panel to agree on which indicators were to be studied. The expert panel concluded that there was no difference between the quality of the two levels of care studied. CONCLUSIONS: Medical audit was a useful method for evaluating medical quality. Co-operation between hospital doctors and general practitioners was of great value for evaluation of the quality of primary health care.

Adult↗
PubMed1996

Synthesis of oligosaccharides corresponding to structures found in capsular polysaccharides of Cryptococcus neoformans--II.

Formula 1 depicts a generalized structure of the capsular polysaccharides of four serotypes of the opportunistic microorganism Cryptococcus neoformans, which appears as one of the major infections in the late stages of development of AIDS. Syntheses are now described of two tetrasaccharides with corresponding structures. These are methyl O-alpha-D-mannopyranosyl-(1-->3)-[O-beta-D-xylopyranosyl-(1-->2)] -O-alpha-D-mannopyranosyl-(1-->3)-alpha-D-mannopyranoside and methyl O-alpha-D-mannopyranosyl-(1-->3)-[O-beta-D-glucopyranosyluronic acid-(1-->2)]-O-alpha-D-mannopyranosyl-(1-->3)-alpha-D-mannopyranoside.

Carbohydrate Conformation↗
PubMed1996

Distribution of keratan sulphate and chondroitin sulphate in wild type and white mutant axolotl embryos during neural crest cell migration.

In embryos of the white mutant axolotl, prospective pigment cells are unable to migrate from the neural crest (NC) due to a deficiency in the subepidermal extracellular matrix (ECM). This raises the question of the molecular nature of this functional defect. Some PGs can inhibit cell migration on ECM molecules in vitro, and an excess of this class of molecules in the migratory pathways of neural crest cells might cause the restricted migration of prospective pigment cells seen in the white mutant embryo. In the present study, we use several monoclonal antibodies against epitopes on keratan sulphate (KS) and chondroitin sulphate (CS) and LM immunofluorescence to examine the distribution of these glycosaminoglycans at initial (stage 30) and advanced (stage 35) stages of neural crest cell migration. Most KS epitopes are more widely distributed in the white mutant than in the wild type embryo, whereas CS epitopes show very similar distributions in mutant and wild type embryos. This is confirmed quantitatively by immunoblotting: certain KS epitopes are more abundant in the white mutant. TEM immunogold staining reveals that KS as well as CS are present both in the basal lamina and in the interstitial ECM in both types of embryos. It remains to be investigated whether the abundance of certain KS epitopes in the white mutant embryo might contribute to the deficiency in supporting pigment cell migration shown by its ECM.

Ambystoma↗
PubMed1996

Effects of extracellular matrix molecules on subepidermal neural crest cell migration in wild type and white mutant (dd) axolotl embryos.

Migration of neural crest (NC) derived pigment cells is restricted in the white mutant (dd) axolotl embryo (Ambystoma mexicanum). Transplantations between mutant and wild type embryos show that the extracellular matrix (ECM) of the white mutant is unable to support the migration of prospective pigment cells in wild type embryos (Löfberg et al., 1989, Dev. Biol. 131:168-181). In the present study, we test the effects of various purified ECM molecules on NC cell migration in the subepidermal migratory pathway of wild type (D/-) and white mutant (dd) axolotl embryos. We adsorbed the ECM molecules onto membrane microcarriers, which were then implanted under the epidermis. Fibronectin (FN), tenascin (TN), collagens I and VI, and a chick aggrecan stimulated migration in both types of embryos. Laminin-nidogen, rat chondrosarcoma aggrecan, and shark aggrecan stimulated migration in dd embryos but did not affect migration in D/- embryos. Collagen III, fibromodulin and bovine aggrecan had no effect on migration in either type of embryo. NC cells did not migrate on control microcarriers, which lacked ECM molecules. Some cells observed contacting, and presumably migrating on, coated microcarriers could be identified as pigment cells by their ultrastructure. Enzymatic digestion in vivo with chondroitinase ABC had no effect on NC cell migration. The neutral or stimulatory effect of the aggrecans is surprising; when tested in vitro they inhibited NC cell migration. The effect of three-dimensionality and other molecules present either in the embryonic ECM or in solution may overcome the inhibitory effect of aggrecans.

Ambystoma↗
PubMed1996

Alleviation of glucose repression of maltose metabolism by MIG1 disruption in Saccharomyces cerevisiae.

The MIG1 gene was disrupted in a haploid laboratory strain (B224) and in an industrial polyploid strain (DGI 342) of Saccharomyces cerevisiae. The alleviation of glucose repression of the expression of MAL genes and alleviation of glucose control of maltose metabolism were investigated in batch cultivations on glucose-maltose mixtures. In the MIG1-disrupted haploid strain, glucose repression was partly alleviated; i.e., maltose metabolism was initiated at higher glucose concentrations than in the corresponding wild-type strain. In contrast, the polyploid delta mig1 strain exhibited an even more stringent glucose control of maltose metabolism than the corresponding wild-type strain, which could be explained by a more rigid catabolite inactivation of maltose permease, affecting the uptake of maltose. Growth on the glucose-sucrose mixture showed that the polypoid delta mig1 strain was relieved of glucose repression of the SUC genes. The disruption of MIG1 was shown to bring about pleiotropic effects, manifested in changes in the pattern of secreted metabolites and in the specific growth rate.

DNA-Binding Proteins↗
PubMed1996

Labor migration as a prelude to World War I.

"At the same time as the political tensions increased in Europe around 1900, an international labor market was developing. More and more proletarians from different parts of the continent searched for labor opportunities in the center of the agrarian and industrial capitalism. In several countries, including Russia, capitalists more and more actively recruited labor migrants for seasonal work. The labor migrants became a political issue as a part of the trade negotiations between Germany and Russia. Also, the Austrian colonization and political expansion in the Balkans can be looked upon in a perspective of (labor) migration. Class and ethnic conflicts coincided and escalated into an international conflict."

Demography↗
PubMed1996

Neural crest cell migration and pigment pattern formation in urodele amphibians.

This review deals with research on the development and differentiation of the neural crest (NC) in amphibians carried out during the past twenty years. First, earlier studies on the migration and differentiation of NC cells in vitro are summarized. These studies include the modes of NC cell migration and their differentiation into chondroblasts, perichondral cells, neurons, Schwann cells and pigment cells (melanophores and xanthophores). Then a summary is given on the development of cranial sensory ganglia and enteric ganglia in Xenopus laevis. In the subsequent sections, mechanisms of NC cell migration are investigated in Ambystoma mexicanum, the Mexican axolotl (wild-type and white mutant) using ultrastructural, immunohistochemical and biochemical methods. In wild-type or dark axolotl embryos, pigment cells leave the NC and migrate out under the epidermis, whereas in the white mutant, pigment cells remain closely confined to the original position of the NC. This system provides an excellent model for analyzing NC cell migration in vertebrate embryos. Further sections deal with the development of larval pigment patterns in Triturus alpestris, (horizontal melanophore stripes) and Ambystoma mexicanum (vertical melanophore bars). Comparing the formation of these patterns shows that two different principles exist in the distribution of pigment derivatives of the NC: patterns following environmental cues (Triturus) and those ignoring these cues, relying solely on cell-cell interactions (Ambystoma). Other studies relate to evolutionary perspectives in pigment pattern formation. They are based on phylogenetic analyses of North American ambystomatids, combined with data on pigment patterns and their formation where such data are available. These studies have shown that vertical bars which develop from aggregates in the NC string are an evolutionary innovation, compared to the more primitive horizontal stripes lacking aggregates in the NC. Thus, in this review we show that the NC of amphibians (T. alpestris, Xenopus laevis, dark and white axolotls and other ambystomatids) may be used for various analyses concerning the migration and differentiation of its derivatives, as well as for studies on the formation and evolution of pigment patterns.

Animals↗
PubMed1994

Regulation of receptor internalization by the major histocompatibility complex class I molecule.

We showed previously that peptides derived from the alpha 1 domain of the major histocompatibility complex class I protein (MHC-I) inhibit internalization of some receptors, thereby increasing the steady-state number of active receptors on the cell surface. In consequence, sensitivity to hormone (e.g., insulin) is enhanced, transport (e.g., of glucose by GLUT-4) is increased, and carrier proteins (e.g., transferrin) operate less efficiently. Now we report that a bioactive peptide (but not closely related inactive ones) binds to MHC-I on the cell surface, not in the groove but apparently to the alpha 1 helix. The binding is saturable, and the number of peptide binding sites on the cell surface approximately equals the number of MHC-I molecules. Antibodies to MHC-I inhibit peptide binding. Most significant, antibodies to MHC-I mimic the effect of a bioactive peptide, inhibiting receptor internalization. These results indicate that MHC-I participates in the regulation of cell surface receptor activity.

Amino Acid Sequence↗
PubMed1994

Altered DNA ligase III activity in the CHO EM9 mutant.

Delayed joining of DNA strand breaks and a high spontaneous level of sister-chromatid exchanges (SCEs) are characteristics of the mutant cell strain EM9 of Chinese hamster ovary (CHO) cells. The introduction of the human gene XRCC1 into EM9 cells reverts the phenotypic properties of EM9 to those of the wild type. We have investigated both DNA ligase activities and a protein which stimulates DNA ligase activity in mutant EM9 cells, XRCC1-transfectant H9T3-7-1 cells and wild-type AA8 cells. Our results, which demonstrate both a decreased DNA ligase activity in EM9 cells using poly(rA).oligo(dT) as substrate and a decreased ability of DNA ligase III to form a covalent DNA ligase III-adenylate intermediate with AMP, clearly indicate an altered DNA ligase III activity in the mutant. Furthermore, the AMP-binding capacity of DNA ligase III and its enzymatic activity with the synthetic polymer were restored after transfection of EM9 with the human XRCC1 gene. Immunoblotting data suggest that the XRCC1 gene does not code for DNA ligase III. In conclusion, the data indicate that the EM9 cell strain has an altered DNA ligase III activity that can be restored by the XRCC1 gene product.

Adenosine Monophosphate↗
PubMed1994

Membrane lipids of adult human brain: lipid composition of frontal and temporal lobe in subjects of age 20 to 100 years.

The membrane lipid composition of human frontal and temporal cortices and white matter has been studied in 118 subjects, age 20-100 years. The brain specimens were selected from subjects who lived a normal social life and died suddenly and unexpectedly with no history of neurologic or psychiatric disease. Macroscopic and microscopic examinations ruled out any signs of organic brain disorder. The sudden death eliminated all risk of changes over a long agonal stage. The data for total solids and major lipids are summarized in graphic form. Total solids, phospholipids, and cholesterol diminished linearly from 20 years of age in frontal and temporal cortices, whereas total solids phospholipids, cholesterol, cerebroside, and sulfatide showed a curvilinear diminution in frontal and temporal white matter. Gangliosides differed from the other lipids, showing an almost constant concentration between 20 and 70 years of age with a slight peak around 50 years of age. The ganglioside pattern showed continuous change with aging, with decreasing proportions of GM1 and GD1a and increasing proportions of GD1b, GM3, and GD3. Equations are given that can be used to calculate the lipid composition of normal human frontal and temporal cortices and white matter at any age between 20 and 100 years of age. These data can be used where data by direct analysis are not available for comparison with values for various pathological states.

Adult↗
PubMed1994

Implementation of a structured care programme for diabetes mellitus in a defined population in mid-Sweden.

A local programme for diabetes care, based on the Swedish national programme, was introduced in the Köping-Arboga-Kungsör area in mid-Sweden in 1984. Before the programme was implemented, a survey of diabetes care was performed in the area. Two years later, a new survey involving 92% of 1253 diabetes patients in the area was performed to see if the programme was associated with an improved level of care, more optimal treatment and better metabolic control. A significant number of Type 2 patients were referred from hospital outpatient clinics to the primary health care centres. The proportion of patients on diet only increased from 26% to 30% and the average number of daily injections among insulin-treated patients increased. The average number of check-ups by a doctor decreased and the number of check-ups by specially trained nurses increased. Overall, the number of check-ups per year increased from 3.1 to 3.8. The proportion of the patients fulfilling the HbA1c criterion of 'good metabolic control' (< or = 6.0%) increased significantly, as did those fulfilling the fasting blood glucose criterion (< or = 7.0 mmol l-1). Serum cholesterol and serum triglyceride levels increased. Relative weight, blood pressure, smoking habits, and exercise habits were unchanged. In conclusion, the quality of diabetes care was improved after the diabetes care programme was implemented.

Adult↗
PubMed1993

Inhibition of internalization of glucose transporters and IGF-II receptors. Mechanism of action of MHC class I-derived peptides which augment the insulin response in rat adipose cells.

Peptides from the alpha 1 domain of the major histocompatibility complex class I antigen (MHC class I), e.g. Dk-(61-85) and Dk-(62-85), have been shown previously to augment glucose uptake in insulin-stimulated cells and to inhibit insulin receptor internalization (Stagsted, J., Reaven, G. M., Hansen, T., Goldstein, A., and Olsson, L. (1990) Cell 62, 297-307). We now report that these peptides inhibit by 80-100% the internalization of glucose transporters (GLUT4) and insulin-like growth factor II (IGF-II) receptors in insulin-stimulated cells and correspondingly double insulin-stimulated glucose transport activity and the number of GLUT4 and IGF-II receptors on the cell surface. In addition, the peptides enhance the apparent affinity about 3-fold of IGF-II binding to its receptor. It is concluded that the effects of the peptides on glucose transport and IGF-II binding are a consequence of the peptide-mediated inhibition of internalization of GLUT4 and IGF-II receptor. The active peptides are derived from the alpha 1 domain of a MHC class I molecule, suggesting that the latter is involved in regulation of internalization of cell surface integral membrane proteins such as the GLUT4 and IGF-II and insulin receptors.

3-O-Methylglucose↗
PubMed1993

Amino acid residues essential for biological activity of a peptide derived from a major histocompatibility complex class I antigen.

The stimulatory activity of peptides from the alpha 1 domain of the major histocompatibility complex (MHC) class I antigen on adipose cell glucose transport was previously shown to require a preformed, ordered conformation of the peptide. The two peptides studied previously were Dk-(61-85) (ERETQIAKGNEQSFRVDLRTLLRYY) and Dk-(69-85). We now show that systematic alanine substitution in Dk-(69-85) identifies residues that are essential for biological activity. Ordered structure of the peptides, estimated by circular dichroism, was found in all peptides with activity, but with a complex variety of spectra. Inactive peptides were in either a random coil or an ordered structure. Ordered structure, therefore, is not sufficient for activity. The peptides self-interact in the absence of cells and form aggregates that precipitate upon centrifugation. The tendency to aggregate is correlated with biological potency. Only MHC class I molecules have significant homology to the peptides studied here. The peptide self-interaction suggests that the biological effects in cells, which result from inhibition of receptor and transporter internalization, may be due to the binding (tantamount to self-interaction) of the peptide to the homologous sequences in the alpha 1 domain of the MHC class I molecule.

Adipose Tissue↗
PubMed1993

Insulinomimetic effect on glucose transport by epidermal growth factor when combined with a major histocompatibility complex class I-derived peptide.

Peptides derived from the alpha 1-region of the murine H-2Dk molecule enhance glucose uptake in rat adipose cells above the maximum obtained with insulin stimulation alone (Stagsted, J., Reaven, G. M., Hansen, T., Goldstein, A., and Olsson, L. (1990) Cell 62, 297-307). We now describe that epidermal growth factor (EGF) in combination with the same peptides, Dk-(61-85) and Dk-(62-85), stimulates cellular glucose uptake 5-7 times over the basal level, i.e. to 30-50% of the maximal insulin effect. EGF alone increased glucose uptake by only approximately 50% above basal and the peptide alone by 100% above basal. Maximal effect of EGF and peptide was reached in 10-20 min with 30 microM peptide (EC50 10-15 microM) and 50 nM EGF (EC50 1-2 nM). The effect of EGF and peptide on glucose uptake was additive to that of insulin and peptide until the maximal level attained with insulin and peptide was reached. The combined effect of EGF plus peptide on glucose transport was associated with a recruitment of GLUT4 molecules to the plasma membrane. However, the phosphatidylinositol (PI) kinase which is activated by insulin was not activated by EGF plus peptide. Thus, the effect of EGF plus peptide on glucose uptake seems independent of the activity status of the insulin receptor. 125I-Labeled EGF bound specifically to rat adipose cells with an apparent affinity of approximately 2 nM and Bmax approximately 5 x 10(3). However, the major histocompatibility complex (MHC) peptides did not affect EGF-stimulated internalization of EGF receptor, in contrast to their effect on the insulin receptors. Transforming growth factor alpha had an effect similar to EGF on glucose uptake. Three other peptides derived from other parts of murine MHC class I had no effect on glucose uptake in combination with EGF. Thus, EGF in combination with certain MHC class I-derived peptides is insulinomimetic concerning glucose transport and this effect is independent of the insulin receptor activity.

3-O-Methylglucose↗
PubMed1993

Characterization of the joining chain (J-chain) promoter.

A 300 b.p. promoter from the mouse joining chain (J-chain) gene was studied with regard to functional activity and protein/DNA interactions. The promoter only stimulated expression of a chloramphenicol-acetyl-transferase (CAT) reporter gene when an enhancer was present in the construct, regardless of whether the construct was transfected into cell lines that did or did not express an endogenous J-chain. Furthermore, deletion mutants lacking the 5' portion of the promoter were transcribed at a higher rate than the intact promoter in both J-chain positive and J-chain negative B-cell lines but not in untransformed B lymphocytes stimulated by lipopolysaccharide, indicating the presence of a negative control element in the 5' portion of the J-chain promoter active in tumour cells only. The octamer element in the J-chain promoter was found to bind Oct proteins, albeit with a low affinity. The penta-deca (p.d.) element in the J-chain promoter bound proteins in extracts from untransformed B cells but not in the tested cell lines. The protein binding to the J-chain p.d. element did not compete efficiently with a p.d. element from the SP6 kappa promoter. A protein binding to the 5' portion of the J-chain was expressed in some cell lines but not in others; neither a negative nor a positive correlation to J-chain expression could be seen. It was concluded that the J-chain promoter is equivalent to a kappa promoter and that differentiation-specific J-chain expression is governed by distal, positive control elements located outside the analysed region.

Animals↗
PubMed1993

Correlation between insulin receptor occupancy and tyrosine kinase activity at low insulin concentrations and effect of major histocompatibility complex class I-derived peptide.

In rat adipocytes, insulin dose-response curves were determined for the following effects in the same cells under the same conditions: glucose uptake, binding to insulin receptors (IR), IR autophosphorylation in vivo and in vitro, IR tyrosine kinase activity and insulin-stimulated phosphatidylinositol (PI) kinase. All the EC50 values were essentially the same (mean +/- S.E.M. was 7 +/- 1 nM), except for glucose uptake, which was 170 pM. Using an improved method, we were able to measure PI kinase activity at picomolar concentrations of insulin (> 30 pM) corresponding to the EC50 for glucose uptake. These experiments showed that insulin-stimulated increase in glucose uptake was associated with an increase in antiphosphotyrosine antibody precipitable PI kinase activity, consistent with the view that IR tyrosine kinase activity may be involved in insulin-mediated signaling of glucose uptake. Small peptides (17-25 residues long) derived from major histocompatibility complex class I have previously been shown to inhibit IR internalization without any effect on the affinity of insulin to the receptor. It is now shown that the peptide-mediated inhibition of internalization, which doubles the number of insulin-occupied receptors at an insulin concentration of 70 pM, also results in a corresponding enhancement of PI kinase activity and glucose uptake. Thus, the receptors arrested on the cell surface by the peptide are biologically active.

1-Phosphatidylinositol 4-Kinase↗
PubMed1992

Tumor-associated antigen 43-9F is of prognostic value in squamous cell carcinoma of the lung. A retrospective immunohistochemical study.

BACKGROUND: Squamous cell lung carcinoma (SLC), the most frequent type of lung cancer, generally is treated surgically and its prognosis is poor. The only current clinically useful prognostic criterion is lymph node staging (TNM classification). Expression of a novel tumor-associated carbohydrate epitope Gal beta 1-3[Fuc alpha 1-4]GlcNAc beta 1-4[Fuc alpha 1-3]GlcNAc beta 1-3 Gal beta 1-4Glc identified by the 43-9F monoclonal antibody (MoAb) is associated with the growth pattern of SLC cell lines in athymic mice and in vitro. This implies that the 43-9F epitope may be related to tumor progression in patients with SLC and that, as such, it could be of prognostic value. METHODS: Primary tumor specimens from 231 patients with lung carcinoma (130 with SLC, 64 with adenocarcinoma, 10 with small cell carcinoma, 16 with large cell carcinoma, and 11 with adenosquamous carcinoma) were examined by immunohistochemical studies on formalin-fixed, paraffin-embedded tissue samples for immunoreactivity with an MoAb to the 43-9F antigen. Univariate and step-wise Cox regression analyses were used to compare survival time by histopathologic diagnosis, smoker status, TNM classification, and type of surgical treatment. RESULTS AND CONCLUSIONS: Patients with 43-9F epitope-positive SLC tumors had a significantly (P less than 0.01) better prognosis than patients with epitope-negative tumors. In contrast, no association was seen between 43-9F epitope expression and survival time for patients with lung adenocarcinomas. Further, the prognostic value of 43-9F expression in SLC was found to be superior to the N-classification with the added advantage that it requires access only to primary tumor tissue and thus is available before therapy.

Adult↗