Retention of nanoparticles-labeled bone marrow mononuclear cells in the isolated ex vivo perfused heart after myocardial infarction in animal model.

Cell therapy of myocardial infarction (MI) is under clinical investigation, yet little is known about its underlying mechanism of function. Our aims were to induce a sub-lethal myocardial infarction in a rabbit, to evaluate the abilities of labeled bone marrow mononuclear cells to migrate from the vessel bed into extracellular space of the myocardium, and to evaluate the short-term distribution of cells in the damaged left ventricle. Sub-lethal myocardial infarction was induced in rabbits by ligation of the left coronary vessel branch (in vivo). The Langendorff heart perfusion model (ex vivo) was used in the next phase. The hearts subjected to MI induction were divided into 3 groups (P1-P3), and hearts without MI formed a control group (C). Nanoparticles-labeled bone marrow mononuclear cells were injected into coronary arteries via the aorta. Perfusion after application lasted 2 minutes in the P1 group, 10 minutes in the P2 and C groups, and 25 minutes in the P3 group. The myocardium of the left ventricle was examined histologically, and the numbers of labeled cells in vessels, myocardium, and combined were determined. The numbers of detected cells in the P1 and C groups were significantly lower than in the P2 and P3 groups. In the P2 and P3 groups, the numbers of cells found distally from the ligation were significantly higher than proximally from the ligation site. Bone marrow mononuclear cells labeled with iron oxide nanoparticles proved the ability to migrate in the myocardium interstitium with significantly higher affinity for the tissue damaged by infarction.

The role of the autonomic nervous system in the etiology of idiopathic scoliosis: prospective electron microscopic and morphometric study.

OBJECTS: The exact etiology of scoliosis is still unknown. The main purpose of this study is to search for the possible causation of scoliosis in the development changes of autonomic nervous structures. In this prospective study, we followed-up the changes in peripheral nerve structures and its discrepancies regarding the concavity and convexity of the scoliotic curve. MATERIALS AND METHODS: We evaluated 12 patients with the idiopathic scoliotic deformity and the control group of 3 patients without any scoliotic deformity. The samples from the peripheral nerves of the convexity and concavity of the scoliotic deformity were drawn during the surgical correction by using the transthoracic approach. The samples were examined by the electron microscopic method and morphometric statistical evaluation. RESULTS: In samples taken from the scoliotic convexity, 23.71% of myelinized nerve fibers (MNF), 12.21% of unmyelinized nerve fibers (UNF), and 5.0% of Schwann cells (SC) were found by the morphometric measurement. There were 17.36% of MNF, 5.82% of UNF, and 5.27% of SC in samples taken from the concavity and 29.9% of MNF, 19.9% of UNF, and 16.7% of SC in the control nonscoliotic samples. Statistically significant differences between both sides of scoliotic deformity (convexity and concavity) and differences between the scoliotic samples and the nonscoliotic control samples were found. In all scoliotic samples, significant morphologic changes were found, mostly in the myelin sheaths and axon fiber abnormalities compression. CONCLUSION: There are significant morphologic changes in spinal autonomic nervous structures in scoliotic patients. These findings can help us in the search for the etiology of scoliosis.

Comparison of the effect of amphotericin B desoxycholate and amphotericin B colloidal dispersion on renal functions and renal morphology in rats.

BACKGROUND AND AIM: Amphotericin B (AmB) desoxycholate remains as one of the most efficacious agents currently available for the treatment of systemic fungal infections; however, amphotericin B colloidal dispersion (ABCD) has been developed because of AmB desoxycholate nephrotoxicity. The goal of our study was to compare the effect of administration of AmB desoxycholate and ABCD on renal functions and renal morphology in rats. RESULTS: Amophotericin B desoxycholate as well as ABCD causes damage to renal tubuli and polyuria. Amophotericin desoxycholate causes considerably more severe damage to tubuli than ABCD, but the morphological damage to renal glomeruli is minimal in both formulas. In tubular cells, AmB desoxycholate causes severe damage to mitochondria, vacuolation of cytoplasm, and increased values of volume density of peroxisomes. CONCLUSION: None of these formulas causes a decrease in glomerular filtration in rats when animals are properly hydrated.

Influence of amphotericin B deoxycholate or amphotericin B colloidal dispersion on renal tubule epithelium in rat.

Amphotericin B deoxycholate (AmB) or Amphotericin B colloidal dispersion (ABCD) are used in clinics for the treatment of systemic fungal infections. The goal of our study was to compare the nephrotoxicity of these drugs in rat kidney. The effects of AmB and ABCD on the ultrastructure of the epithelium of renal tubules were studied and evaluated using morphometric and statistical methods. Two groups of 3 animals were established: group 1 was treated with AmB desoxycholate and group 2, to which ABCD was applied. AmB caused more than ABCD ultrastructural changes in the cytoplasm of the epithelial cells: damage to mitochondria, vacuolation of cytoplasm, and increased values of volume density of peroxisomes. However, we failed to observe significant differences in morphology and density of the other cell organelles. The proximal tubules seemed to be more sensitive to the nephrotoxic influence of both formulas than the distal tubules of rat kidney. Although, AmB causes more severe damage than ABCD, both drugs cause damage to renal tubuli.

Cytochalasin D interferes with contractile actin ring and septum formation in Schizosaccharomyces japonicus var. versatilis.

The cells of Schizosaccharomyces japonicus var. versatilis responded to the presence of cytochalasin D (CD), an inhibitor of actin polymerization, by the disappearance of contractile actin rings (ARs) that had already formed and by inhibition of new ring formation. Actin cables disappeared. Actin patches remained preserved and became co-localized with regions of actual cell wall formation (at cell poles and at the site of septum development). Removal of the AR arrested formation of the primary septum and led to the production of aberrant septum protrusions in that region. Nuclear division was accomplished in the presence of CD but new ARs were not produced. The wall (septum) material was deposited in the form of a wide band at the inner surface of the lateral cell wall in the cell centre. This layer showed a thin fibrillar structure. The removal of CD resulted in rapid formation of new ARs in the equatorial region of the cells. This implies that the signal for AR localization was not abolished either by CD effects or by removal of an AR already formed. Some of the newly developed ARs showed atypical localization and orientation. In addition, redundant, subcortically situated actin bundles were produced. The removal of CD was quickly followed by the development of primary septa co-localized with ARs. Wall protrusions occurred co-localized with the redundant actin bundles. If these were completed in a circle, redundant septa developed. The AR is a mechanism which, in time and space, triggers cytokinesis by building a septum sequentially dependent on the AR. Aberrant septa were not capable of separating daughter cells. However, non-separated daughter cells subsequently gave rise to normal cells.