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B Nico

Publications and source records attributed to B Nico.

102 records · Page 6Linked to original sources

Blood vessel ultrastructure in the chick optic tectum developing under chronic hypoxia conditions.

The maturation process of blood vessels has been ultrastructurally investigated in the optic tectum of chick embryos kept in a condition of aerogenic hypoxia and of chickens born from fertilized eggs incubated under hypoxia but kept in the open air after hatching. By comparing the fine structure of the intratectal vessels of chick embryos exposed to hypoxia to that of embryos developed under normal conditions, the conclusion has been drawn that O2 deprivation does not prevent the temporal sequence of appearance and/or differentiation of the various vascular wall components (endothelium, endothelial basement lamina, pericytes, perivascular glia), but it produces, at least in a part of the latter, modifications, the type and degree of which apparently depend upon hypoxia duration.

Animals↗

[Effects of chronic hypoxia on microcirculation of the central nervous system during embryonic development].

In the attempt to know the factors influencing the vasculogenesis and to verify whether the vessel formation and growth are influenced, during different ontogenetic periods, by oxygen deficiency, the intraneural vascular network has been morphometrically analyzed in chicken embryo optic tectum under conditions of aerogenic hypoxia. Chicken eggs, incubated under routine conditions, have been half-painted with melted wax at the 2nd incubation day (i.d.). Fragments of optic tectum, isolated from living embryos at the 8th, 14th and 17th i.d., have been fixed and embedded according to the usual E/M procedures. A parallel series of normally developed embryos of 8, 14 and 17 incubation days has been likewise prepared. On semithin sections from the hypoxic specimens and normal control embryos the area occupied by vessels (Av), the number of vessels (Nv) and the diameter of the radially directed ones (Dv) have been evaluated. The preliminary results indicate that hypoxia evokes, from the 8th to the 17th i.d., an increment of the Av parameter, due first to microvessel neoformation and enlargement from the 8th to the 14th i.d., then from the 14th to the 17th i.d. only to a growth of new capillary branches. The response of the vascular network to the hypoxic condition is more marked from the 8th to the 14th i.d., t.i. when, in relation to the differentiation and the stratification of the neurons, the metabolic requirements of the developing tectum are presumably increased. O2 deficiency causes severe developmental disorders of the cyto- and mieloarchitecture of the tectum: the vascular response can apparently prevent actual damages only when the hypoxic condition lasts for a relatively short time.

Animals↗

[Structural modifications of medullary bone osteoclasts during a hypocalcemic diet].

The medullary bone of laying hens after seven days of hypocalcaemic diet has been investigated with the aim of analyzing the fate of osteoclasts, very numerous in the first days of the diet and after substituted on the trabecular surfaces by active osteoblasts. The first observations show that there is a marked change in the osteoclasts ultrastructure. Large amount of endoplasmic granular reticulum in regular rows are accumulated at the cell periphery. Cytoplasmatic blebs, microvilli and laminae ondulantes are visible on the cell surfaces. Mononuclear cells with variable amount of cytoplasm rich in organuli are detached from osteoclasts. The ultrastructure and the fate of this elements are discussed.

Animals↗

Angiogenesis spectrum in the stroma of B-cell non-Hodgkin's lymphomas. An immunohistochemical and ultrastructural study.

Samples of lymph nodes from 88 patients with B-cell non-Hodgkin's lymphoma (B-NHL) grouped by the Working Formulation (WF) and from 15 patients with benign lymphadenopathies were investigated immunohistochemically and ultrastructurally for changes in angiogenesis and stromal distribution of two subendothelial basement membrane (BM) components, namely laminin and type IV collagen. The microvessel number was usually low in lymphadenopathies, and increased significantly in low-grade B-NHL. Intermediate-grade tumors displayed a further significant increase that was mainly due to their diffuse subtypes rather than to the follicular subtype. High-grade B-NHL showed the highest counts. By contrast with the lymphadenopathies studied, the stroma of B-NHL reacted intensely with both BM components, whose linear co-expression was significantly associated with low-grade and follicular intermediate-grade B-NHL, while expression of laminin alone in a granular pattern was detected in diffuse intermediate-grade and high-grade tumors. Ultrastructural analysis revealed immature vessels more frequently in diffuse intermediate-grade, and in high-grade B-NHL. These in situ data suggest that angiogenesis occurring in B-NHL increases along their progression path, and emphasize the importance of angiogenesis as an epigenetic phenomenon of B-NHL progression.

Analysis of Variance↗

Cell-mediated delivery of fibroblast growth factor-2 and vascular endothelial growth factor onto the chick chorioallantoic membrane: endothelial fenestration and angiogenesis.

Fibroblast growth factor-2 (FGF2) and vascular endothelial growth factor (VEGF) exert their angiogenic activity by interacting with endothelial cells in a distinct manner. In this study, we investigated the morphological features of endothelial cells of the chick embryo chorioallantoic membrane (CAM) microvasculature after stimulation with FGF2 or VEGF. In order to provide a continuous delivery of the growth factor, we utilized a recently developed gelatin sponge/CAM assay in which a limited number of FGF2- or VEGF-transfected cells were adsorbed onto gelatin sponges and applied on the top of the CAM on day 8 of development. Their angiogenic activity was compared to that exerted by a single bolus of the corresponding growth factor. All the angiogenic stimuli induced a comparable vasoproliferative response, as demonstrated by the appearance of similar numbers of immature blood vessels within the sponge on day 12. No angiogenic response was observed in CAMs implanted with the corresponding parental cell lines or vehicle. Electron microscopy demonstrated that VEGF-overexpressing cells modified the phenotype of the endothelium of the blood vessels at the boundary between the implant and the surrounding CAM mesenchyme. The endothelial lining of 30% of these vessels showed segmental attenuations, was frequently interrupted and became fenestrated, mimicking what is observed in tumor vasculature. In contrast, the vessels consisted of continuous endothelium sealed by tight junctions in all the other experimental conditions. These results indicate that FGF2 and VEGF interact with endothelial cells of the CAM in a distinct manner. Both growth factors induce a potent angiogenic response, but only VEGF delivered in a continuous manner by its transfectants can modify the phenotype of the otherwise quiescent endothelium of CAM blood microvessels. The gelatin sponge/CAM assay may constitute a new model to study the mechanisms leading to endothelial fenestration in tumor growth.

Adsorption↗

Effects of Aroclor 1254 on intercellular communication in human keratinocytes.

It has been previously described that Aroclor 1254 can inhibit GJIC in rodent liver cells where it is known to be a tumor promoter, while the possibility that Aroclor 1254 exerts its inhibitory effects on GJIC in human keratinocytes and acts as a human skin tumor promoter, deserves further attention. In the present study the effects of Aroclor 1254 were examined on gap junction channel permeability, on connexin 43 (Cx 43) expression at mRNA and protein level and on ultrastructural modification to add further experimental evidence to its inhibitory effect on GJIC. The results were compared to those induced by 12-O-tetradecanoylphorbol-13 acetate (TPA), a tumor promoter known to be a potent inhibitor of GJIC in human skin cells and to those induced by benzo[a]pyrene (B[a]P) known for its genotoxic activity. Our data show increased Cx 43 protein expression in Aroclor 1254 and TPA-treated cultures compared to controls, decreased Cx 43 protein level in those exposed to B[a]P, while Cx 43 gene expression (Cx 43 mRNA) was unaffected by the treatments. In Aroclor and TPA-treated keratinocytes, the ultrastructural examination showed residues of junctional systems expressed by specular, short tracts of the faced plasma membranes. In contrast, the contacts between plasma membranes of adjacent B[a]P treated keratinocytes were more extended. A clear inhibition of gap junction channel permeability due to Aroclor 1254 and TPA was also manifest by Lucifer yellow dye test compared to B[a]P-treated cultures where dye spreading to the neighbouring cells and to the extracellular space occurred. The present data, in addition to confirming inhibition of GJIC mediated by Aroclor 1254 in human keratinocytes, which were found to be comparable to those induced by TPA, suggest that GJIC inhibition is associated with increased Cx 43 protein expression without significant modification of its gene expression.

Analysis of Variance↗

[Neurotoxic effect of 7,8-oxide styrene on striatal neuron culture].

The present study was undertaken to test the hypothesis that the neurotoxic action of styrene may be primarily presynaptic in nature and may involve impaired regulation of DA content and stimulation of DA release. Primary striatal neurons were grown in vitro and exposed to styrene oxide at different concentrations to evaluate the minimal effective dose able to induce these synaptic alterations.

Animals↗

Ultrastructure and permeability of immature neural and extraneural blood vessels.

The ultrastructure and permeability to the marker horseradish peroxidase in the leptomeningeal and neural vessels of the optic lobes, and in the wing bud vessels, were compared, during early stages of chick embryo vasculogenesis, in order to ascertain whether young neural vessels, like mature ones, possess structural specificity preventing the free transport of molecules through their wall (blood-brain barrier). The results demonstrated that immature endothelia are always permeable to the tracer, since the marker passes the vessel wall through the interendothelial clefts (paracellular route) as well as by endo-exocytotic mechanisms (transcellular route). Nevertheless, the transport by vesicles is somewhat reduced in the neural vessels compared to that in the extraneural ones, suggesting that the former may be influenced by the surrounding neuropile to differentiate in a specific manner right from early development.

Animals↗

[Ultrastructure of the myocardial junctions of the chick embryo at an early stage in the organogenesis of the heart].

The ultrastructural features of the myocardiocyte junctional systems have been studied in the heart right myocardium of 6 day chick embryos in order to analyze the relationships between the spatial arrangement of the myocardial fibres and the formation of the myocardiocyte junctions. The myocardiocytes are remarkably branched, joined in small fibres to form a loose network with large intercellular spaces and appear well differentiated, rich in organelles, myofibrils and glycogen. Adherent-type junctions and well differentiated desmosomes are detectable at the level of the termino-terminal contacts between myocardiocytes, where the plasma membranes appear more or less complicately interconnected; nexus-type junctions are seen in the latero-lateral contact regions. The results indicate that already at an early stage of the heart organogenesis the myocardium intercellular junctions are similar, on the whole, to those described in the adult, so that they would not seem to be transitory or modifiable structures. The changes in the spatial orientation of the myocardial fibres, which take place after the 6th incubation day, could be allowed by the network-like arrangement of the primitive myocardium and presumably conditioned by the blood flow in the developing heart.

Animals↗

[Apoptosis or programmed cell death: regulatory and pathophysiological mechanisms].

Apoptosis is an active death process genetically encoded to eliminate abnormal or unwanted cells. The phenomenon is induced by a cascade of molecular events leading to nucleolysis by endonucleases and involves a number of membrane receptors and cytoplasmic proteins. These structures (including Fas, müllerian inhibiting substance, p53 and the c-myc oncogene) contribute, by interactive regulatory mechanisms, to the promotion or inhibition of apoptosis, on the basis of both external stimulus and cell activation state. Since apoptosis is a selective process to suppress defective cells, deregulation of genes encoding for such apoptosis-related proteins could be relevant in the growth of several tumors. Remarkably, overexpression of the bcl-2 gene in a few experimental lymphomas has been associated with neoplastic proliferation because of its inhibitory effect on apoptosis. Conversely, early activation of Fas, an apoptosis-inducing gene on HIV-infected CD4+ lymphocytes, is thought to aggravate T cell lymphopenia in HIV infection by increasing the level of normal apoptosis. Genetic deregulation of apoptosis has also been postulated in the pathogenesis of several diseases. Indeed, while preliminary studies suggest that apoptosis plays a role in autoimmune disorders including systemic lupus erythematosus, the pathogenesis of a few degenerative neuropathies, such as Alzheimer's disease, could depend on a similar altered mechanism in apoptosis of neuronal cells. However, no studies are presently available to suggest that exploitation of molecular events of apoptosis would imply therapeutic progress.

Acquired Immunodeficiency Syndrome↗

Lymph node angiogenesis in lymphoproliferative disorders: type II Mixed cryoglobulinemia as a model.

OBJECTIVES: Lymph node biopsies from patients with mixed cryoglobulinemia (MC) were investigated for: a) the presence of the hepatitis C virus (HCV) peptides C22 and C100; b) the degree of angiogenesis and of inflammatory infiltrate (macrophages and neutrophils); c) the distribution of laminin and type IV collagen, the main components of the subendothelial basement membrane; and d) the ultrastructural characteristics of the microvessels. METHODS: Cryostat sections were stained by immunoperoxidase to highlight HCV peptides, endothelial cells, their basement membrane components, and inflammatory cells. Planimetric methods were applied to count the microvessels and inflammatory cells, and to evaluate the distribution pattern of the basement membrane components. Microvessels were also analysed at the ultrastructural level. RESULTS: HCV+ lymph nodes showed higher microvessel and inflammatory cell counts than the HCV- lymph nodes. Their laminin and type IV collagen distribution and ultrastructural findings also indicated immature capillaries. CONCLUSIONS: HCV could be introduced into the lymph nodes by infected mononuclear cells, and trigger inflammation and angiogenesis, thus contributing to the inflammatory process. Angiogenesis, in turn, could facilitate HCV dissemination and persistence in MC.

Biopsy↗