Biomedical subjects

G Stoica

Publications and source records attributed to G Stoica.

76 records · Page 5Linked to original sources

PubMedDate not supplied

Immunohistochemical localization of proliferating cells, basic fibroblast growth factor and Fos protein following iliac artery balloon angioplasty in hypercholesterolemic rabbits.

The restenotic process in iliac arteries of hyperlipidemic rabbits following balloon angioplasty was evaluated in a temporal sequence by monitoring smooth muscle cell (SMC) proliferation (proliferating cell nuclear antigen -PCNA marker), growth factor (basic fibroblast growth factor -bFGF) production, and Fos oncogene protein expression using immunohistochemical methods. The percutaneous transluminal angioplasty was performed in iliac artery of rabbits fed a 1% cholesterol diet, with a balloon catheter inflated from 4 to 8 atm for 2 min under cineangiographic control until an acceptable (at least 50% stenosis reduction) result was obtained. The morphometric analysis indicated that the number of PCNA-positive cells in contralateral control arteries was low, but was increased in balloon-injury. The bFGF-positive labeled cells were localized in the media and in recently-migrated SMCs within the intima. Two days following angioplasty these cells were more abundant and scattered in the entire neo-intima. After 14 days their number was still higher than that of the controls. Cellular Fos protein expression was detected in the intima and, to a lesser extent, in the media 2 hours after angioplasty. These data suggest that early expression of Fos protein and bFGF in iliac arteries of hyperlipidemic rabbits following balloon angioplasty could be involved in development of restenosis in this animal model.

Alkaline Phosphatase↗

PubMedDate not supplied

Evaluation of potential oncogene alterations in the ENU1564 rat mammary tumor model.

The ENU1564 tumor line originated from a rat mammary tumor induced by N-ethyl-N-nitrosourea (ENU), an alkylating chemical carcinogen which induces genetic point mutations. The oncogene abnormalities in rat mammary tumors induced by ENU have not been characterized. In this study, two highly metastatic clones (Br7-C5 and FP2-All) derived from the adenocarcinoma cell line ENU1564, were evaluated for the presence of mutational activation involving the c-Ha-ras, c-neu, and p53 oncogenes. These oncogenes were chosen for investigation based upon their involvement in other ENU-induced rat tumors (c-neu in malignant schwannomas and p53 in nephro-blastomas) or in methylnitrosourea (MNU)-induced rat mammary tumors (c-Ha-ras). Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and sequence-specific oligonucleotide hybridization analyses indicated that no c-Ha-ras codon 12 mutation was present in these tumor cells. PCR-RFLP and single-stranded conformational polymorphism (PCR-SSCP) analyses showed that no sequence changes were present over a 138 base-pair gene fragment spanning codon 664 of the c-neu protooncogene (the site of point mutation in ENU-induced rat nerve tumors). Immunoprecipitation and Western immunoblotting indicated that the p53 protein is neither over-expressed nor mutated in the tumor cells. The results failed to identify specific oncogene alterations in the ENU1564 rat mammary tumor line but ruled out mutational activation of c-Ha-ras (codon 12), c-neu (codon 664), and the p53 genes.

Adenocarcinoma↗

PubMedDate not supplied

Sarcoma viruses containing the mos oncogene induce lesions resembling Kaposi's sarcoma.

Kaposi's sarcoma is most accurately described as a multifocal angioproliferative lesion primarily involving the skin, although some studies indicated concomitant and/or exclusive visceral involvement. The mechanism(s) involved in Kaposi's sarcoma development, especially AIDS multiorgan distributed form, is not completely understood. Recent reports have identified a murine retrovirus, MoMuSV-349 that induces multiorgan disseminated angiosarcomatous tumors which resemble Kaposi's sarcoma when virus is inoculated intraperitoneally in newborn BALB/c mice. Performed time point experiment on mice infected with MoMuSV-349 indicated a two stages development of Kaposi's sarcoma-like tumors; sarcomatous and angiosarcomatous. Preliminary studies have demonstrated the pathogenesis of the disease process and the role of angiogenic growth factors released by the spindled cells in the stage development of mouse tumors. It is hypothesized that growth factors such as fibroblast growth factors released by the spindled cells stimulate the proliferation of endothelial cells and neovascularization which is an essential component of Kaposi's sarcoma-like tumors. Understanding the mechanism(s) of endothelial cells proliferation and neovascularization as a response to viral insult and microenvironmental changes will raise the possibilities of developing new therapeutic approaches to block this process.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

Quantitative variation of free amino acids in the central nervous system of MoMuLV-ts1-infected mice.

A temperature-sensitive mutant of Moloney murine leukemia virus (MoMuLV-ts1) induces polioencephalomyelopathy and hind limb paralysis in highly susceptible FVB/N strains of neonatal mice. This disease is characterized by progressive motor neurons loss and severe gliosis within specific target areas of the central nervous system (CNS). The mechanism(s) of this neurodegeneration is unknown. In the neonatal infection of the CNS, the MoMuLV-ts1 virus was reported to replicate within the endothelial, ependymal, astrocytes and microglial cells. Since no virus or viral products were recognized in the degenerating neurons, it is postulated that an indirect mechanism(s) caused the loss of neurons in the neonatally infected mice. This study was undertaken to investigate the possible pathogenic role of excitatory amino acids (EAAs) such as glutamate and other nonneurotransmitters amino acids (NAAs) in this animal model. The free amino acids concentration was analysed by a fluorometric HPLC method. The temporal measurements of the free amino acids concentration, glutamate, glutamine and arginine from the brain stem and spinal cord of MoMuLV-ts1-infected mice was significantly decreased when compared with the control non-infected mice. The concentration of EAAs during the course of this infection indicated a sharp decline in glutamate and its precursor, glutamine with early infection (10 days post infection-dpi). This deficiency persisted (20 and 30 dpi) in the spinal cord, where the neuronal loss was most severe, but not in the brain stem. A similar pattern occurs with the amino acid arginine. These observations suggest that an astrocyte-induced metabolic disturbance of glutamate and arginine in the CNS of developing mice, could be, in part responsible for the loss of motor neurons observed in this model.

Amino Acids↗