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Biomedical subjects

U Lindberg

Publications and source records attributed to U Lindberg.

At least 91 records · Page 5Linked to original sources
PubMed1981

Characterization of platelet extracts before and after stimulation with respect to the possible role of profilactin as microfilament precursor.

The amount of profilactin in platelet extracts made in the absence of free Ca++ ions decreases and the amount of free profilin increases as a consequence of thrombin stimulation. This agrees with the proposed role of profilactin as a microfilament precursor in nonmuscle cells. Filamentous actin in extracts of unstimulated platelets appears partly in large aggregates that contain actin binding protein (ABP) and relatively few other proteins. After stimulation, the amounts of actin and ABP in the aggregates are increased and myosin is also included together with a few additional proteins. When the cells are lysed in the presence of Ca++, aggregation is drastically reduced. The data indicate that filamentous actin depolymerizes rapidly and recombines with available profilin, and that a Ca-specific interaction also occurs between actin and a new protein with molecular weight about 90,000.

Actins↗
PubMed1981

On the ultrastructural organization of the microfilament system and the possible role of profilactin.

This paper summarizes results of studies on human glia cells concerning the ultrastructural relationships in the microfilament system and the possible role of the profilactin complex. It presents electron micrographs of the leading lamella of cells grown on solid substratum, visualizing the organization of the microfilament system in this highly motile part of the cell at high resolution and at what appears to be a high level of preservation. These results are linked to observations made in our laboratory of the biochemical basis for the dramatic rearrangements occurring in platelets in response to thrombin stimulation. Taken together these results lead to a relatively detailed model for the mechanism of cell motility.

Actins↗
PubMed1981

Antibodies to lipid A during urinary tract infection.

Serum levels of antibodies to lipid A were determined with an enzyme-linked immunosorbent assay in 26 girls with their first known symptomatic urinary tract infection (UTI) and in 15 girls with asymptomatic bacteriuria (ABU). Also included were six female patients with recurrence of acute upper UTI, five of whom had renal changes after the infections; 28 female patients with renal scarring but not symptomatic UTI at the time of investigation; and uninfected individuals. IgG and IgM antibodies to lipid A were found in approximately 50% of the uninfected children older than two years of age. Girls with acute cystitis, acute pyelonephritis, or ABU showed significantly elevated levels of IgG antibodies to lipid A as compared with children with no history of UTI. High levels of IgG antibodies to lipid A may be indicative of severe renal infection and development or progression of renal parenchymal reduction. The diagnostic value of determining levels of antibodies to lipid A is discussed.

Adolescent↗
PubMed1981

Mild mental retardation in Swedish school children. I. Prevalence.

In an unselected series of Swedish school children born 1966-70, the prevalence of mild mental retardation, defined as an IQ of 50-70, was determined. A prevalence of 0.4% was revealed. The findings in this study, supported by recent IQ analyses in other Scandinavian countries, indicate that a true prevalence for the IQ range 50-70 was ascertained. The high average social standard and early social stimulation are put forth as a likely explanation for the low prevalence of mild mental retardation in Swedish preschool and school children.

Child↗
PubMed1981

Mild mental retardation in Swedish school children. II. Etiologic and pathogenetic aspects.

The etiology and pathogenesis of mild mental retardation (MMR) (IQ 50--70) were analysed in an unselected series of 91 Swedish school children with this condition born 1966--70. The cause was considered to be prenatal in 23%, including 5% genetic, prenatal unknown in 10% and alcohol fetopathy in 8%. A perinatal cause--mainly asphyxia combined with fetal deprivation--was found in 18% and a postnatal in 2%. In 55% the cause was untraceable. Half of these latter children had close relatives with below-average intelligence. Exceptionally low birth weights and lengths were revealed among the 8% with alcohol fetopathy. Neurological abnormalities were found in 43% of the children, epilepsy in 12%, cerebral palsy in 9% and a clumsy child syndrome in 23%. Psychiatric disturbances were present in 31%.--The types and multitudes of predisposing background factors in MMR were compared with those in severe mental retardation and with those in the IQ group 71--75. The general conclusion is drawn that in Swedish school children negative pre- and perinatal factors are today responsible for a larger proportion of MMR than has previously been known.

Asphyxia Neonatorum↗
PubMed1981

Adhesion, hemagglutination, and virulence of Escherichia coli causing urinary tract infections.

The capacity of 453 Escherichia coli strains to agglutinate erythrocytes and yeast cells and to attach to human urinary tract epithelial cells was tested. The strains were isolated from the urine of patients with acute pyelonephritis, acute cystitis, or asymptomatic bacteriuria and from the stools of healthy school children. Three main patterns of hemagglutination were found: (i) mannose-resistant agglutination of human erythrocytes alone or simultaneously with mannose-sensitive agglutination of guinea pig erythrocytes; (ii) only mannose-sensitive agglutination of guinea pig and other erythrocytes; and (iii) no agglutination. Strains with mannose-resistant agglutination of human erythrocytes alone or in combination with mannose-sensitive hemagglutination attached in high numbers to human urinary tract epithelial cells. Bacteria inducing only mannose-sensitive hemagglutination attached in low numbers, and non-agglutinating strains did not bind to the urinary tract epithelial cells. The bacterial surface antigen(s) mediating mannose-resistant hemagglutination of human erythrocytes and attachment to human urinary tract epithelial cells may be one factor selecting for E. coli from among the fecal flora which infect the urinary tract. The highest proportion of strains with this property was found among acute pyelonephritis isolates (77%), and the lowest proportion of strains with this property was found among normal fecal E. coli (16%).

Agglutination↗
PubMed1981

Early noise-induced hearing loss in teenage boys.

A hearing examination of 538 teenage boys in vocational school classes--implying future on-the-job noise exposure--showed a hearing loss (greater than 20 dB HL at any frequency) in 15% of the cases. Few correlations could be demonstrated between hearing loss and specific leisure time activities. There was, however, a correlation between high frequency hearing loss in the left ear and hereditary hearing loss. The most affected frequency was 6 kHz, suggesting a noise etiology--a suggestion emphasized by the noisy hobbies of these teenagers. It cannot be excluded that a hereditary deficiency could either manifest itself as a localized dip at 6 kHz or reveal itself as an increased vulnerability to noise, identified at young age as a high frequency dip at 6 kHz.

Adolescent↗
PubMed1980

Visualization of the peripheral weave of microfilaments in glia cells.

A peripheral weave of microfilaments is visualized in human glia cells. In this weave small numbers of microfilaments converge to structures in the cell edge. Similar assemblies of microfilaments seem to be attached to structures on the surface of microspikes. Together with filaments splaying from the paracrystalline arrangement in microspikes, these units make up the peripheral weave. The filaments of the weave come in close contact with each other and with filaments of internal actin fibres.

Actins↗
PubMed1979

Adhesiveness to urinary tract epithelial cells of fecal and urinary Escherichia coli isolates from patients with symptomatic urinary tract infections or asymptomatic bacteriuria of varying duration.

Adhesiveness to human urinary tract epithelial cells was high for Escherichia coli strains isolated from patients with acute pyelonephritis and acute cystitis, and low for asymptomatic bacteriuria strains detected at screening. Escherichia coli bacteria causing asymptomatic reinfections, detected near the onset of bacteriuria, adhered more than those detected at screening. No difference in the adhesive ability was found between fecal isolates of the strain causing urinary tract infection, isolated at or before onset of bacteriuria, and the urinary strain in symptomatic or asymptomatic patients. Normal fecal Escherichia coli from non-bacteriuric patients adhered less than all other strains tested.

Adhesiveness↗
PubMed1979

Reorganization of actin in platelets stimulated by thrombin as measured by the DNase I inhibition assay.

The effect of thrombin stimulation on actin organization in human platelets has been analyzed by using the DNase I inhibition assay, which is selective for unpolymerized and filamentous actin. The results provide biochemical evidence for the suggestion that stimulation leads to rapid polymerization of actin. The measurements also reveal changes in the polymerization state of actin occurring after cell lysis. These changes are influenced by the concentration of free calcium in the extracts.

Actins↗
PubMed1979

The unpolymerised form of actin in non-muscle cells.

Several lines of evidence point to the existence of unpolymerised actin in non-muscle cells. Ultrastructural examination reveals both a variety of actin filament bundles and actin in a controversial organisational state. Arguments are cited that this material, which at least in part is found close to the plasma membrane, represents unpolymerised actin rather than a random array of single actin filaments. The rearrangement of actin filament bundles during the cell cycle, and in response to experimental manipulation, suggests a turnover of filaments by a polymerisation-depolymerisation cycle. Extracts made from non-muscle cells under conditions where muscle actin would polymerise still contain appreciable fractions of monomeric actin. Studies on purified polymerisation-resistant actin from a variety of sources reveal the presence of a small protein which binds specifically to actin and prevents polymerisation. In the last section of the article, we expand the idea that this auxiliary protein is a central control element in the regulated exchange between non-polymerised and polymerised actin in vivo.

Actins↗