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Biomedical subjects

I Julkunen

Publications and source records attributed to I Julkunen.

102 records · Page 6Linked to original sources
PubMed1983

Chondroitin sulfate at the plasma membranes of cultured fibroblasts.

We have previously shown that in confluent human fibroblast cultures chondroitin sulfate proteoglycan is a component of the fibronectin-containing pericellular matrix fibers. In the present work the distribution of chondroitin sulfate was studied in subconfluent cell cultures using antibodies that bind to a chemically defined carbohydrate fragment of chondroitinase ABC-modified chondroitin sulfate proteoglycan. Using immunofluorescence microscopy, we observed, in addition to the fibrillar matrix staining, chondroitin sulfate diffusely distributed at the cell surface. In indirect immunoferritin electron microscopy this staining corresponded to patchy binding of ferritin close (24 nm) to the outer aspect of the plasma membrane. The patchy organization appeared uniform in all cell surfaces. The cell surface chondroitin sulfate could not be removed from the plasma membrane by agents that dissociate electrostatic interactions. These data show that in fibroblasts chondroitin sulfate is a component of the outer aspect of the plasma membrane, and raise the possibility of an integral plasma membrane chondroitin sulfate proteoglycan.

Animals↗
PubMed1983

Interaction of viral envelope glycoproteins with fibronectin.

An interaction between fibronectin and viral envelope glycoprotein micelles isolated from influenza A, parainfluenza 1, and mumps viruses was found by enzyme immunoassay. All three different glycoprotein micelles bound efficiently to solid-phase fibronectin. When fibronectin was permitted to bind to solid-phase viral glycoproteins, dose-dependent binding was observed. Soluble glycoprotein micelles inhibited the binding of fibronectin to immobilized glycoprotein preparations. The binding was not observed when fibronectin was pretreated with neuraminidase, suggesting that the sugar moieties of fibronectin are responsible for the affinity. This affinity may play a role in virus-cell interactions or in the opsonization of certain viruses during infection.

Fibronectins↗
PubMed1982

Chronic encephalomyelitis with specific increase in intrathecal mumps antibodies.

Symptoms of severe encephalomyelitis developed in a 31-year-old man in 1967. He had a high serum antibody titre to mumps virus associated with a polymorphic cell reaction and an increased protein concentration in cerebrospinal fluid (CSF). He recovered considerably within a year and was able to resume work. In 1975 his condition deteriorated again; it improved during the following few years, but a further deterioration then occurred. In March, 1981, the complement-fixing antibody titre to mumps virus was 1/32 in the serum and 1/4 in the CSF. In November, 1981, the CSF IgG index was increased and the altered serum/CSF antibody ratio persisted. The specificity of the altered antibody ratio was confirmed by the single radial haemolysis test and an immunoassay specific for mumps virus. Antibodies against the mumps virus envelope glycoprotein, M-protein, and nucleoprotein could be demonstrated by immunoprecipitation and the antibody patterns in serum and CSF were similar. Antibodies against other microorganisms were not detected in the patient's CSF, and mumps antibodies were not found in the CSF specimens of 57 control patients. This case may be an example of a new disease-chronic mumps virus infection in the central nervous system.

Adult↗
PubMed1982

Sensitive interferon assay based on immunoenzymatic quantification of viral antigen synthesis.

A sensitive enzyme immunoassay (EIA) for determining the biological activity of human interferon was developed. Green monkey kidney (Vero) cells and human embryonic lung (HEL) cells were grown in microtitre plates, treated with leukocyte interferon (IFN alpha) and infected with vesicular stomatitis virus (VSV). Cells were fixed with paraformaldehyde and permeabilized with Triton X-100. Viral antigen synthesis was measured by labelling the cells with VSV antiserum followed sequentially by protein A horseradish peroxidase conjugate and o-phenylenediamine. Interferon activity was detected as a lowering of the absorbance value from that of the virus control wells, reflecting the inhibition of virus protein synthesis by interferon. The minimum amount of interferon producing statistically significant (P less than 0.01) decrease of absorbance in Vero cells was 1-5 international units (I.U.)/ml as in the standard plaque reduction test the detection limit was 7.5 I.U./ml or more. In HEL cells the detection limit was 1 I.U./ml measured by EIA. The EIA for interferon activity is at least as sensitive as the traditional plaque reduction test. It is reproducible, easy to automatise and requires 7-10 times less cell culture materials than the plaque reduction test. We find it preferential especially when large numbers of specimens with limited volumes are to be analysed for interferon activity.

Animals↗
PubMed1982

Immune complexes in serum and cerebrospinal fluid of multiple sclerosis patients and patients with other neurological diseases.

Paired serum and cerebrospinal fluid (CSF) specimens from 30 multiple sclerosis (MS) patients and 30 patients with other neurological diseases (ONDs) were analyzed for the presence of immune complexes (ICs). With each of the 4 tests used, ICs were found more frequently in sera from both MS and OND patients than in sera from healthy blood donors. IC-positivity for MS and OND patient CSF varied from 10-33% and from 10-17% in different tests. The number of IC-positive sera or CSF in MS patients did not differ significantly from those in OND patients. For both MS and OND patients, the positivity pattern for serum and CSF specimens in each IC test was essentially unique. Furthermore, because several CSF IC-positive and serum IC-negative paired specimens were found, intrathecal IC formation may be independent of IC formation in peripheral blood. The presence of ICs in serum or CSF did not correlate with the clinical status of or laboratory data on the MS patients, nor was a correlation found with the diagnosis of the OND patients. In total, these results suggest that the presence or absence of ICs in MS or OND patients may simply reflect changes in the immunological regulation of individual patients.

Adult↗
PubMed1981

Etiological, social and therapeutical aspects of osteoarthrosis and soft-tissue rheumatism in a Finnish health centre material.

A study of 690 osteoarthrosis (OA) patients with corresponding controls, and 475 soft-tissue rheumatism (STR) patients with the same number of controls was made in Finnish health centres. The aim of the study was to clarify certain etiological, social and therapeutical aspects. No clear differences were found in the working conditions of patients with OA, STR, or their controls, or in their occupational classes. OA patients were less satisfied with their working conditions than were the other. OA and STR patients had been more actively engaged in sports earlier in life, but during the study there were no differences; nor did the localisation of OA differ. The weight index qas slightly higher in OA, particularly when knee and ankle were affected, but not with arthrosis of the hip. There were no clear associations with other diseases. The maximum duration of a treatment period in this study was 1 month. The average sick leave in OA was 17.8 days, in STR 13.4 and in controls 15.4 days. After treatment, 31% of OA patients, and 56% of STR were recommended to resume work; 4% were recommended to change their occupation; 21% of OA and 7% of STR patients were recommended to retire on pension. Sulindac, indomethacin and many other drug combinations were used for medication. Certain side effects were found in about 5% of sulindac- and in 8-10% of indomethacin-treated patients. In 17% of OA and in 12% of STR patients, it was found necessary to consult a specialist for diagnosis or treatment.

Body Weight↗
PubMedDate not supplied

Etiology of central nervous system infections in the Philippines and the role of serum C-reactive protein in excluding acute bacterial meningitis.

OBJECTIVES: The value of measurements of serum C-reactive protein (CRP) in differentiating central nervous system (CNS) infections of varying etiologies in the Philippines was investigated. METHODS: A wide array of bacteriologic and virologic methods as well as computed tomography, typical clinical presentation, and autopsy were used for etiologic diagnosis. RESULTS: Among 103 patients with CNS infection, etiology was identified in 60 (58%) cases. Bacteria were found in 19 (including 7 Streptococcus pneumoniae, 5 Haemophilus influenzae, 3 Neisseria meningitidis), tuberculosis in 4, viruses in 38 (including 20 coxsackievirus, 8 measles, 4 adenovirus, and 4 poliovirus infections), and brain abscess in 3 patients. C-reactive protein was elevated on admission in all 18 cases of bacterial meningitis tested, exceeding 50 mg/L in 17 (94%), and was not affected by prior antibacterial treatment. The mean CRP was significantly higher in the bacterial group than in the viral group (207 +/- 111 mg/L vs. 39 +/- 34 mg/L; P < 0.001). In the viral group one third had CRP above 50 mg/L. In patients with tuberculous meningitis, brain abscess, or cryptococcal meningitis, CRP was moderately to highly elevated. CONCLUSIONS: In the presence of a normal CRP concentration (below 10 mg/mL) acute bacterial meningitis is excluded even in a developing country setting and antimicrobial therapy is not warranted.

Acute Disease↗
PubMedDate not supplied

Molecular pathogenesis of influenza A virus infection and virus-induced regulation of cytokine gene expression.

Despite vaccines and antiviral substances influenza still causes significant morbidity and mortality world wide. Better understanding of the molecular mechanisms of influenza virus replication, pathogenesis and host immune responses is required for the development of more efficient means of prevention and treatment of influenza. Influenza A virus, which replicates in epithelial cells and leukocytes, regulates host cell transcriptional and translational systems and activates, as well as downregulates apoptotic pathways. Influenza A virus infection results in the production of chemotactic (RANTES, MIP-1 alpha, MCP-1, MCP-3, and IP-10), pro-inflammatory (IL-1 beta, IL-6, IL-18, and TNF-alpha), and antiviral (IFN-alpha/beta) cytokines. Cytokine gene expression is associated with the activation of NF-kappa B, AP-1, STAT and IRF signal transducing molecules in influenza A virus-infected cells. In addition of upregulating cytokine gene expression, influenza A virus infection activates caspase-1 enzyme, which is involved in the proteolytic processing of proIL-1 beta and proIL-18 into their biologically active forms. Influenza A virus-induced IFN-alpha/beta is essential in host's antiviral defence by activating the expression of antiviral Mx, PKR and oligoadenylate synthetase genes. IFN-alpha/beta also prolongs T cell survival, upregulates IL-12 and IL-18 receptor gene expression and together with IL-18 stimulates NK and T cell IFN-gamma production and the development of Th1-type immune response.

Animals↗
PubMedDate not supplied

Fibronectin and viral pathogenesis.

Fibronectin is a dimeric high-molecular-weight glycoprotein composed of two similar but not identical subunits. Differences have been observed between plasma and cell-derived fibronectins, and molecular and sequencing studies have revealed a domain structure. The characteristic features of fibronectin include its various molecular and biologic interactions, which can be assigned to the different domains of the molecule. Fibronectin was originally discovered as a protein missing from the surfaces of virus-transformed cells. The importance of functional oncogenes in the loss of extracellular matrices was later established in a number of studies using virus mutants that are temperature-sensitive for transformation. The loss of the extracellular matrix appears to be a result of multiple events in cells but is not a prerequisite for malignant growth in vivo. There appear to be multiple transformed phenotypes, and the loss of extracellular fibronectin may be due in part to proteolytic activity by the cells and other alterations caused by functioning oncogenes. The wide distribution of tissue and soluble forms of fibronectin offers multiple occasions for interactions with other molecules. Binding of fibronectin to viruses and purified viral proteins has been observed in a number of studies. Neuraminidase-sensitive virus-binding sites in the fibronectin molecule have tentatively been identified. Fibronectin also is capable of binding to various complement components, possibly making clearance of viral antigen-antibody-complement complexes, which are observed in the circulation during viral infection, more rapid. The virus-binding ability of fibronectin may play a role in modifying viral infections in the body.

Animals↗
PubMedDate not supplied

C3c-binding in inflammatory rheumatic diseases.

Sera from 73 patients, 24 with rheumatoid arthritis (RA), 10 with Sjögren's syndrome (SS, 4 with and six without RA), 17 with Reiter's syndrome (RS), 10 with systemic lupus erythematosus (SLE), 9 with Yersinia arthritis (YA), and 3 with mixed connective tissue disease (MCTD) were examined by enzyme-immunoassay (EIA) for the presence of C3c-binding IgG, IgM, and IgA activity (C3cBIgG, C3cBIgM, C3cBIgA). This activity probably consists of immunoconglutinins and immunoglobulin aggregates. Significantly elevated C3cBIgG was found in the sera of patients with RA (p less than 0.01), SS, and SLE (p less than 0.02). C3cBIgM was elevated in SS and SLE (p less than 0.02). C3cBIgA was increased in RA (p less than 0.005), in SS and YA (p less than 0.02). Correlations of C3c-binding with erythrocyte sedimentation rate, hemoglobin, C-reactive protein, IgG-binding onto platelets, serum IgG, IgM, and IgA levels, and with rheumatoid factors of IgM and IgA classes were computed. C3cBIgG, C3cBIgM, and C3cBIgA correlated significantly with each other, but usually not with other laboratory variables. The exceptions were positive correlations of C3cBIgM with IgM-rheumatoid factors in RA (p less than 0.05), and with serum IgM levels in the whole series of patients (p less than 0.05). The use of C3c represents a new principle to detect abnormalities in the sera of patients with inflammatory rheumatic diseases. However, the pathogenic significance of elevated C3c-binding remains unknown.

Complement C3↗