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Biomedical subjects

L Mori

Publications and source records attributed to L Mori.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Dilated cardiomyopathy and visceral anomalies in myotonic dystrophy].

In dystrophia myotonica clinical evidence of cardiac involvement usually appears several years after the onset of neuromuscular symptoms. In more than 90% of cases there is damage to the specialized cardiac tissues and in about 7% of cases there are alterations to the myocardium. We report a case characterized by early and spread deterioration of the pump function developing into refractory congestive heart failure. The contemporary involvement of the smooth muscle of gallbladder and colon confirms the hypothesis that dystrophia myotonica is a pan-muscle disease.

Aged↗
PubMed1989

Monokine production by microglial cell clones.

Cytokines have been suggested to act as intermediates between the immune and the central nervous system, but little is known about the type of cells synthesizing them in the brain. We have immortalized with oncogenic retroviruses primary brain cell cultures from mouse embryos and have generated clones of microglial cells that have been characterized. Three of the clones studied produce interleukin 1 (IL 1); IL 6 and tumor necrosis factor-alpha as assessed by biological assays and by Northern blot analysis. Our data raise the question on the role of these cytokines in the brain and suggest that early resident microglial cells might play an important role in development processes and in the adult brain.

Animals↗
PubMed1989

Generation of new oncogenic murine retroviruses by cotransfection of cloned AKR and MH2 proviruses.

We have obtained a set of oncogenic recombinant retroviruses, the 3RV complex, by cotransfecting murine fibroblasts (SC-1 cells) with plasmids containing the cloned genomes of the avian MH2 and murine AKR viruses. The transfected culture (TAM-2) was shown to release murine transforming viruses by means of reverse transcription and focus formation assays. Analysis of TAM-2 intracellular RNA revealed new transcripts hybridizing with the oncogenes myc and mil and cross-hybridizing with an AKR probe. The biological activity of the 3RV complex was tested for the induction of murine macrophage proliferation in the absence of exogenous growth factors, a property described as the result of mil and myc cooperativity. Cell-free supernatants from 3RV transformed fibroblasts were indeed able to induce the proliferation of macrophage-like cells from murine bone marrow and spleen primary cultures. Such cultures were capable of continuous growth and showed independence from exogenous myeloid growth factors. The cells expressed antigenic markers and functional properties specific of the monocytic-macrophage lineage. These results suggest that transfection-induced recombination could be a novel way to generate biologically active recombinant retroviruses.

Animals↗
PubMed1985

Rearrangement and expression of the antigen receptor alpha, beta and gamma genes in suppressor antigen-specific T cell lines.

The rearrangement and transcription of the antigen receptor alpha, beta and gamma genes were investigated in murine antigen-specific suppressor T cell lines, to establish whether the suppressor T cell subset expresses the same antigen receptor transcripts previously found in helper and cytotoxic T lymphocytes. The genomic organization of the alpha, beta and gamma chain loci was investigated using probes representative of the entire gene or fragments from variable, joining and constant regions. The present results show that in functional suppressor T cells the three antigen receptor genes are all rearranged. The beta gene is expressed in all the tested cell lines, while the expression of the alpha and gamma genes is variable. In one cell line (LH8) alpha and gamma genes are not efficiently transcribed; in the other cell line (LA41) the gamma mRNA is found in amounts similar to beta mRNA, whereas the alpha gene is expressed at low levels. These data suggest that in suppressor T cells no direct correlation exists between the expression of alpha, beta and gamma antigen receptor genes and the effector function.

Animals↗
PubMed1985

Staphylococcus aureus-induced suppression of contact sensitivity in mice: suppressor cells elicited by polyclonal B-cell activation are regulated by idiotype--anti-idiotype interactions.

Staphylococcus aureus strain Cowan I, a strong polyclonal B-cell activator (PBA), inhibited contact sensitivity to oxazolone in mice when administered 24 hr before sensitization. This suppression was mediated by idiotype-positive (Id+) B lymphocytes, which arose very early during the sensitization process and induced anti-Id B cells. These cells were found at Day 3 of the sensitization process and exerted their effect by activating antigen-specific suppressor T lymphocytes, which affected the efferent phase of the immune response. S. aureus strain Wood 46, which lacks of the ability to act as a PBA, was unable to inhibit contact sensitivity. These results indicate that PBA may play an important role in the regulation of cell-mediated immune reactions.

Animals↗
PubMed1985

Polyclonal B cell activators inhibit contact sensitivity to oxazolone in mice by potentiating the production of anti-hapten antibodies that induce T suppressor lymphocytes acting through the release of soluble factors.

Polyclonal B cell activators (PBAs) such as purified protein derivative, lipopolysaccharide, Staphylococcus aureus strain Cowan I (StaCwI), and Pseudomonas aeruginosa inhibit contact sensitivity to oxazolone in mice when given 24 h before sensitization. This suppression, transferable from immunodepressed animals to oxazolone-sensitized recipients with immune serum, has been shown to be due to the early appearance of anti-hapten antibodies. These antibodies elicit T suppressor cells which release soluble factor(s) capable of inhibiting the passive transfer of contact sensitivity.

Animals↗
PubMed1984

T suppressor cells as well as anti-hapten and anti-idiotype B lymphocytes regulate contact sensitivity to oxazolone in mice injected with purified protein derivative from Mycobacterium tuberculosis.

Purified protein derivative from Mycobacterium tuberculosis inhibits contact sensitivity to oxazolone in mice when given intravenously 24 to 72 h before the antigen. Transfer experiments showed that various types of suppressor cells occurred in the lymph nodes draining the site of sensitization: (i) anti-oxazolone idiotype + B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients at the moment of their sensitization; (ii) anti-idiotype B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients when sensitization of these animals had been performed 3 days before cell transfer; (iii) T lymphocytes, found only at day 6 after sensitization, inhibited the passive transfer of contact sensitivity, indicating that they were effective on the efferent phase of the immune response. These results indicate that purified protein derivative from M. tuberculosis interferes with contact sensitivity by activating a complex and multiple immunoregulatory circuit.

Animals↗
PubMed1984

Staphylococcus aureus inhibits contact sensitivity to oxazolone by activating suppressor B cells in mice.

Killed Staphylococcus aureus strain Cowan I cells inhibit contact sensitivity to oxazolone in mice, when given intravenously 24-72 h before sensitization. With transfer experiments it was found that the cells responsible for the suppression are antigen-specific, nylon-adherent, resistant to antitheta serum + C, and sensitive to anti-mouse Ig serum + C. These suppressor B cells bear anti-oxazolone immunoglobulins and appear to exert their suppressive activity by preventing the contact sensitizer from reaching the specific reactive T cells.

Animals↗
PubMed1982

Detection of ischemic myocardial injury in patients with normal, or moderately elevated, serum CK and AST activities.

It is still undecided in clinical medicine if an increased serum CK-MB level indicates irreversible myocardial damage. We measured CK and AST activities on three serum samples obtained during the first 24 hours following admission of patients with a clinical history suggesting myocardial ischemia. Isoenzymes were not separated when CK and AST activities were less than 300 U/L and 35 U/L respectively, but were fractionated when the enzyme activities doubled during the first 24 hours even within their normal ranges. Over a three-year period this doubling occurred in 30 patients, one of whom was admitted twice to the hospital. The serum CK-MB fractions of these patients were 6% or greater in 26 and less than 6% in 5 admissions. The final clinical diagnosis given to the patients on 20 of these 26 admissions was acute subendocardial infarction. None of the five patients with a CK-MB fraction less than 6% had a clinical diagnosis of acute myocardial infarction. A comparative study of 102 patients with higher average enzyme activities but without doubling of both enzymes during a 24-hour period, did not yield a CK-MB of 6% or greater. None of this group of patients was diagnosed clinically as having had acute myocardial infarction.

Aspartate Aminotransferases↗
PubMed1981

Ferrozine iron and total iron-binding capacity method adapted to the ABA-100 Bichromatic Analyzer.

A sensitive method (Clin. Chem. 26: 327--331, 1980) for serum iron, in which the color reagent Ferrozine is used, is modified and adapted to the Abbott ABA-100 discrete analyzer. The standard curve is linear to at least 10 mg/L and the method showed day-to-day precision (CV) of 2.4% for a 1.03 mg/L sample (n = 63) and 1.9% for a 2.13 mg/L sample (n = 63). Lower values were obtained than with the modified continuous-flow technique of Giovanniello et al., but the correlation was good (r = 0.98). Bilirubin and copper do not interfere; hemoglobin and gross lipemia interfere only slightly. The total iron-binding capacity, based on Ramsay's method, was evaluated with regard to the effect of adding various amounts of magnesium carbonate. Results led us to use a ratio of approximately 180 mg of magnesium carbonate to each 5 micrograms of excess iron added. Day-to-day, the method for total iron-binding capacity gave a CV of 3.1% for a 2.55 mg/L sample, 2.8% for a 3.63 mg/L sample.

Autoanalysis↗