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Biomedical subjects

L Accinni

Publications and source records attributed to L Accinni.

At least 19 recordsLinked to original sources
PubMed1988

On the mechanism of action of lonidamine: a study on human erythrocyte membrane.

The incubation of human erythrocytes with increasing levels of the antineoplastic drug Lonidamine clearly indicated a dose-dependent effect on the lipid composition of the plasma membranes. A selective transfer of phosphatidylcholine and cholesterol from membrane to incubation medium and the consequent enrichment in phosphatidylethanolamine of the membrane itself was observed. Moreover, the membranes were found to contain increasing levels of the drug which was incorporated at a constant membrane/medium partition ratio. The changes in composition appeared to be consistent with morphological alterations observed by scanning and freeze-fracture electron microscopy demonstrating changes in cell shape, the presence of numerous intracellular vesicles, and a membrane protein rearrangement. The analysis of intact red cells by nuclear magnetic resonance ruled out the possibility that the alterations described above could be due to an ATP depletion. This further confirmed that cell membranes were the primary target of the Lonidamine action, the previously described energy metabolism impairment being a consequence of a selective damage of cellular membranes, probably originating from the incorporation of the drug into the lipid bilayer.

Cholesterol↗
PubMed1988

Effects of radiofrequency radiation on rabbit kidney: a morphological and immunological study.

The histopathology of the acute and chronic kidney reaction to low-frequency nonionizing electromagnetic radiation was evaluated in New Zealand white rabbits treated with multiple exposure to 27.12-MHz radiofrequencies. At the end of treatment, the animals exhibited focal tubular necrosis and focal and segmental glomerular sclerosis which in a few months evolved into a membranous nephropathy. The latter was characterized by a diffuse, granular localization of rabbit gamma-globulin and complement in most glomeruli and by electron-dense deposits in the subepithelial zone of the glomerular capillary walls, suggesting that these glomerular changes are induced by the localization of antigen-antibody complexes. The data obtained provide strong evidence for the potential nephrotoxicity of radiofrequency radiation and indicate that these nonionizing types of radiation may be capable of eliciting autoimmune phenomena that are likely responsible for the evolution of renal disease in rabbits.

Animals↗
PubMed1987

Cell membrane changes induced by lonidamine in human erythrocytes and T lymphocytes, and Ehrlich ascites tumor cells.

Lonidamine, a derivative of indazol carboxylic acid, has been found to exert a powerful inhibitory effect on oxygen consumption and aerobic glycolysis of neoplastic cells through mechanisms yet to be defined. Recent freeze-fracture studies have shown that Lonidamine alters the distribution of intramembranous particles in the plasma membrane, suggesting that the cell membranes, rather than the energy metabolism, are the drug's primary target. The present study was carried out to further evaluate the effects of Lonidamine on cell membranes, using normal human erythrocytes and T lymphocytes and Ehrlich ascites tumor cells as cell models. These studies indicate that plasma and mitochondrial membranes are the primary site of the drug's action, though other cell membranes seem to be affected as well. Thus, Lonidamine inhibition of energy metabolism in nucleated cells reported in previous studies must be considered as a consequence of the structural damage of the inner and outer mitochondrial membranes, which in turn affects respiration and glycolysis and then cell viability.

Animals↗
PubMed1985

Immunofluorescence study of thymuses of mice given Friend leukemia virus: conventional vs monoclonal antibodies.

In the course of a study of the early effects of Friend Leukemia Virus (FLV) infection in thymus structure and function, evidence of early localization of infectious FLV in the thymic type I and type II epithelio-reticular cells of susceptible mice was obtained. Such evidence was based upon bio-assay, ultrastructural and immunofluorescence observations. As for the latter, conventional monospecific sera against FLV p30 and gp70 antigens as well as two distinct monoclonal antibodies recognizing FLV gp70 epitopes were employed. Both monoclonal antibodies stained with a granular pattern the cytoplasm of type I and II epithelio-reticular cells from susceptible mice injected with live FLV. On the contrary, conventional monospecific sera diffusely stained the cytoplasm of all epithelio-reticular cells of the thymus, independently of mice inoculation with and susceptibility to virus, possibly recognizing tissue-associated normal mouse antigens and/or cross-reacting antigens of other ecotropic viruses.

Animals↗
PubMed1983

Actin in the extracellular matrix of smooth muscle cells. An immunoelectron microscopic study.

Actin has been specifically detected in the intercellular matrix of mouse smooth muscle cells and along the vascular internal elastic membrane by means of immunoferritin-electron microscopy, employing human antibodies to smooth muscle actin. The presence of actin in the smooth muscle matrix suggests that this protein may have relevance in controlling cell-to-cell adhesion and the sliding of one smooth muscle cell over the other, both in contracted and expanded status. The association of actin with the elastic membrane may represent the anatomical basis of a functional link between elastic membrane, adjacent fibronectin and smooth muscle cells. Thus the transmission of movement from the smooth muscle cells to the elastic membrane can be achieved.

Actins↗
PubMed1983

Effects of in vivo Friend leukemia virus infection on levels of serum thymic factors and on selected T-cell functions in mice.

The levels of serum thymic factor(s) (STF), of Thy-1.2 positivity of splenocytes [as measured by their azathioprine (AZ) sensitivity], and of Thy-1.2-positive "spontaneous" spleen rosette-forming cells (SSRFCs), as well as the presence of infectious virus in the thymus, were assessed as a function of time after virus inoculation in susceptible DBA/2, partially resistant BALB/c, and fully resistant C57BL/6 mice given the polycythemia- or anemia-inducing strain of Friend leukemia virus (FLV-P and FLV-A, respectively). As early as Days 2 to 3, the levels of STF and of AZ sensitivity of splenocytes were profoundly decreased in DBA/2 mice, and, to a lesser extent, in BALB/c mice given FLV-P; however, SSRFCs/spleen were increased in both mouse strains. Conclusive evidence of infectious FLV-P was obtained in the thymuses of DBA/2 mice soon after infection. In mice of the same strains infected with FLV-A, STF levels were similarly decreased, but AZ sensitivity of splenocytes was unaffected, and SSRFCs were decreased. Evidence of early FLV-A infection in the thymus of DBA/2 mice was likewise obtained. In C57BL/6 mice given FLV-A, STF levels, AZ sensitivity of splenocytes, and SSRFC showed changes similar to, but of lower magnitude than, those in BALB/c mice. On the other hand, in C57BL/6 mice given FLV-P, the decrease in STF and AZ sensitivity was almost as pronounced as in susceptible DBA/2 mice in the face of complete absence of infectious virus or viral markers in the thymuses. The observed changes are ascribed to virus infection in view of the following: (a) good temporal correlation between these changes and virus infection; (b) absence of any change in mice given heat-inactivated viruses or spleen homogenate of normal DBA/2 mouse spleen; (c) overall good correlation between mouse genotype and genetic (Fv-1 and Fv-2) restrictions of virus infection on one hand and the magnitude of the observed changes on the other. In particular, the decrease in STF and SSRFC levels is ascribed to the replication-competent (Friend-murine leukemia virus) component of Friend leukemia virus complex, whereas the decrease in AZ sensitivity of splenocytes and the increase of SSRFCs are ascribed to the defective spleen focus-forming virus component of the complex. All changes described so far were transient, since they were not detectable beyond 42 days after virus inoculation in overtly leukemic animals. The observed derangements of thymus-derived immune functions may play an important cofactor role during the onset of leukemia in mice genetically permissive to Friend leukemia virus replication and transformation, but they do not seem relevant to the maintenance of leukemia.

Animals↗
PubMed1980

Morphological, immunochemical, and biochemical study of rabbit achilles tendon at various ages.

UNLABELLED: With aging, rabbit tendon tissue undergoes a series of morphological and biochemical changes which involve both the cells and the extrace-lular matrix. The extracellular matrix increases in volume, causing a relative decrease of the number of cells per unit of tissue surface. The tenoblasts become longer and more slender, while their cytoplasmic processes increase in number and become thinner and more elongated, forming a dense network. In addition, tendon cells show a marked decrease in the intracytoplasmic organelles responsible for protein synthesis, while their intracellular content of contractile proteins does not change. With aging collagen fibers increase in diameter and vary more in thickness. These morphological changes correspond to biochemical changes that include an increase in collagen, a decrease in mucopolysaccharides, and a decrease in water content. During aging parallel changes occur in the elastic fibers, which decrease in number and show structural alterations. CLINICAL RELEVANCE: Ultrastructural and biochemical studies of tendon diseases need a normal comparison. Out ultrastructural and biochemical findings in aging tendon may be useful in that regard. The presence of actin and myosin in tendon cells could be related to some aspects of tendon physiology and pathology.

Achilles Tendon↗
PubMed1980

Deposition of immune complexes in ovarian follicles of mice with lupus-like syndrome.

The occurrence of immune deposits in the ovaries of mice with lupus-like syndrome was studied by immunofluorescence, light microscopy, and electron microscopy. Granular deposits of mouse IgG and C3, and occasionally gp70 and denatured DNA, were found in the zona pellucida of mature and atretic follicles. Dense deposits of foreign material were seen by light and electron microscopy in areas of ZP corresponding to the immune deposits. These lesions, presumably induced by immune complexes, resemble the "membranous" changes observed in the glomerular basement membrane in some of the same mice. Inflammatory changes of the ovarian follicles were not observed. The study of "membranous" immune complex oophoritis could contribute to the understanding of immunologic mechanisms of the female reproductive system.

Animals↗
PubMed1979

Degenerative vascular disease and myocardial infarction in mice with lupus-like syndrome.

The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy, and electron microscopy. Medium and small coronary arteries and arterioles of both infarcted and noninfarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid--Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation, and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3, and occasionally gp70 were present in the walls of medium and small arteries, arterioles, and venules of both infarcted and noninfarcted myocardium. Dense deposits of foreign material were found by electron microscopy in areas corresponding to the immune deposits. These findings are consistent with the interpretation that these noninflammatory vascular lesions are caused by local deposition of antigen--antibody complexes. The immune-complex--mediated injury appears to lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.

Animals↗
PubMed1978

Regeneration of rabbit calcaneal tendon: a morphological and immunochemical study.

The regenerated tissue which fills the gap between the stumps of sectioned and unsutured rabbit calcaneal tendon was studied by immunofluorescence, light and electron microscopy from 2 days to 30 weeks after surgery. In the early stages, the newly formed tissue consisted of few connective tissue cells of variable shape dispersed in an abundant intercellular matrix. At 7 days after tenotomy most of the cells were spindle shaped and arranged along the major tendon axis. They showed a well developed rough endoplasmic reticulum, a prominent Golgi complex and bundles of thin and thick filaments. Moreover, they appeared intensely stained when treated with anti-actin and anti-myosin sera. The bulk of the intercellular matrix consisted of bundles of collagen fibers, mostly arranged parallel to the cells. In the subsequent stages the regenerating tissue became more compact, acquiring the morphological characteristics of tendon tissue. At 30 weeks after tenotomy, however, it did not show yet the typical texture of the normal adult tendon. The tenocytes were more numerous and less uniformly distributed, and contained a greater amount of ergastoplasm and contractile proteins. The collagen fibers were similar in size to those of the neonatal normal tendon and the elastic fibers appeared often immature.

Actins↗
PubMed1978

Deposition of circulating antigen--antibody complexes in the gastrointestinal tract of rabbits with chronic serum sickness.

The possible role of circulating immune complexes (IC) in the production gastrointestinal lesions was studied in rabbits with chronic serum sickness (CSS) induced by multiple daily injections of bovine serum albumin (BSA). All rabbits generating a marked antibody response developed IC glomerulonephritis. In approximately 50% of these rabbits granular deposits of BSA, rabbit IgG, and C3 were also found in the gastrointestinal tract. The immune deposits in the gastrointestinal tract were mainly present in the vessel walls, close to the intestinal glands and the surface epithelium, and between the smooth muscle cells. This was accompanied by slight to moderate edema of the mucosa and the submucosa and mild infiltration of inflammatory cells. Electron-densedeposits were found in a pattern corresponding to that observed for BSA, rabbit IgG, and C3. Degranulated neutrophils, basophils, and mast cells were noticed in the interstitium. The presence in the same areas of granular deposits of BSA, IgG, and C3, corresponding to electron-dense deposits, suggests that the deposits contain BSA-anti-BSA complexes. These findings show that in rabbits with CSS circulating IC may localize and induce injury in the gastrointestinal tract.

Animals↗
PubMed1978

Receptors for fluoresceinated human thyroglobulin in peripheral blood lymphocytes.

Fluoresceinated human native and desialylated thyroglobulin were incubated with peripheral blood lymphocytes. 1% of the lymphocytes, in twenty samples from normal human blood donors, showed a bright granular fluorescence where neither the number nor pattern of fluorescence differed from lymphocytes from the blood of thyroiditis patients. Fluoresceinated albumin and gamma-globulin did not bind to the lymphocytes, and a 500-fold excess of native non-fluoresceinated thyroglobulin inhibited the binding and pre-incubation with anti-IgM serum abolished it. Binding with desialylated thyroglobulin was negligible, and the pattern of fluorescence was pale and uniform. Analysis by sucrose gradient centrifugation and double diffusion in agar gel showed that fluorescein dissociates thyroglobulin into 12S fragments and reduces its immunoreaction with autoantibodies. It can therefore be concluded that the 12S molecule produced by fluoresceination maintains its determinants for lymphocyte receptors, whereas further dissociation, as in desialylated fluoresceinated thyroglobulin, leads to a marked reduction in the binding with lymphocytes.

Binding Sites, Antibody↗
PubMed1977

Contractile filaments in cells of regenerating tendon.

An extensive cytoplasmic fibrillar system has been observed in fibroblast-like cell of regenerating tendon. It consists of bundles of actin filaments, which often show a cross-striated appearance due to electron dense bodies occurring throughout their length. The functional role of this contractile apparatus seems to be related to the process of movement and orientation of the newly formed cells and to the retraction of the regenerating tendon.

Animals↗
PubMed1975

Immunoelectron microscopic evidence of contractile proteins in the cellular and acellular components of mouse kidney glomeruli.

Actin and/or actin-like protein have been localized in the cellular and acellular components of the glomerular walls of mouse kidney by means of immunoelectron microscopy, employing human antibodies to smooth muscle (SMA). Contractile antigens have been confirmed to be present in the cytoplasm of podocytes and mesangial cells in association with fine filaments which are considered of importance in the control of blood flow, intravascular pressure, and filtration rate within the glomerulus. The extracellular presence of contractile proteins in the mesangial matrix and glomerular basement membrane can be related to cell movement in a frictional environment. This latter phenomenon, which is strictly interdependent with cell adhesion and aggregation, is most evident in the mesangial cells in a form of luminar pseudopodia, cytoplasmic projections, and phagocytosis.

Actins↗