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Biomedical subjects

R Bona

Publications and source records attributed to R Bona.

26 records · Page 2Linked to original sources
PubMed1990

Persistence of azacytidine-induced SCEs and genomic methylation in CHO cells in vitro.

Many carcinogenic agents are able to affect the methylation level in mammalian cells cultivated in vitro. The capacity of azacytidine (AZA) to demethylate DNA can be used to examine the relationship between the genomic methylation level and cytogenetic end-points. Here we compared the sister-chromatid exchange (SCE) level with the genomic % methylcytosine in a Chinese hamster ovary cell line in vitro after giving a single 10-microM pulse of AZA. Both parameters were followed up to 16 cell cycles after the agent was removed. While the SCE level increased starting 2 cycles from the treatment and persisted for the entire 16 cycles, the methylcytosine level, after an initial 50% decrease, approached the control value, completely returning to it after 10 cell cycles. The possibility that the persistence in the SCE increase is an inherited phenomenon is discussed.

5-Methylcytosine↗
PubMed1990

Retinoids as modulators of metabolism: their inhibitory effect on cyclophosphamide and 7,12-dimethylbenz[a]anthracene induced sister chromatid exchanges in a metabolically competent cell line.

Recently, retinoids have been studied for their ability to modify the carcinogenic/mutagenic activity of chemical compounds. Results show that they can inhibit the malignant transformation of cells, the induction of cancer in experimental animals and the mutagenicity of promutagens. Our experiments examine how retinol and retinoic acid can decrease the frequency of sister chromatid exchange (SCE) induced by two indirect mutagens/carcinogens (cyclophosphamide and 7,12-dimethylbenz[a]anthracene) in an epithelial liver cell line of male Chinese hamster (CHEL cells). These cells are metabolically competent and activate different classes of promutagens into biologically active metabolites. Our results are consistent with the suggestion that retinoids modulate the genotoxicity of indirect-acting mutagens by altering their metabolic activation or cellular detoxification processes or both.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1987

Tissue factor apoprotein: intracellular transport and expression in shed membrane vesicles.

We have studied the synthesis and subcellular distribution of the glycosylated membrane protein tissue factor (TF) in human blood monocytes and the inducible monocyte like cell line, HL-60. Following induction with endotoxin or the phorbol ester, TPA, tissue factor specific activity was measured in intact cells, sonicated cells, isolated plasma membranes and shed vesicles. We have shown that TF is transported over time from the cytoplasm to the plasma membrane and finally to shed membrane vesicles. Optimal transport of TF to the plasma membrane and shedding in membrane vesicles required glycosylation as judged by partial inhibition of this process by the tunicamycin homologues B2 and C2.

Apoproteins↗
PubMed1981

[Active tuberculosis unsuspected until autopsy].

A series of 3195 necropsies performed in cases of natural death at the "S. Giovanni" Hospital in Turin, and covering the years 1969-1978, was studied for the prevalence of active tuberculosis. Active tuberculosis was found in 61 cases (1,9%); in 60 a complete clinical history was available. Forty-two out of these 60 cases (70%) were diagnosed only at autopsy, with higher frequency in the old patients. In the 42 patients with undiagnosed active tuberculosis, the acid fast bacilli resulted to have been searched for only in 3 cases, and a chest-film was recorded in 23 cases; in 27 cases of this group, the period between the admission and the death was longer than 8 days (mean 29 days). The clinical diagnosis of active tuberculosis displays intrinsic difficulties; however it must be stressed that an higher proportion of cases could be recognized if one keeps in mind the possibility of this polymorphic disease, so that adequate clinical, laboratory and x-ray investigations should carried out.

Adult↗
PubMedDate not supplied

Influence of spermidine on sister chromatid exchanges induced by alkylating agents in mammalian cells in vitro.

Sister chromatid exchanges (SCEs) are a very sensitive genetic end-point for in vitro identification of presumed carcinogenic and mutagenic agents, although the mechanism of their formation is still to be elucidated. The present work shows the influence of spermidine on SCE induction by two different DNA damaging agents: Mitomycin-C (MMC) and N-Methyl-N'-Nitro-N-Nitrosoguanidine (MNNG). The SCE level induced by MMC was significantly decreased by spermidine. On the contrary, MNNG-induced SCEs were not affected. It has recently been suggested that MMC, via its reduced metabolite mitosene, produces bulky mono-and bi-adducts in DNA, mainly located in the minor groove of the double helix. MNNG, instead, directly methylates several electrophilic sites of DNA bases, such as the N7 and the O6 of guanines and the N3 of adenines. Both MMC and MNNG, despite their different mechanism of action, are potent SCE inducers. Spermidine, similarly to its structural analogue Spermine, is known to interact with DNA phosphate groups and to bind reversibly to the minor groove, thus stabilizing the double helix structure. Spermidine, being therefore ineffective on the MNNG-mediated DNA methylation, might affect DNA, making it structurally unavailable for MMC binding.

Animals↗
PubMedDate not supplied

[Cerebral cysticercosis: report of a case and review of the literature].

A case of cysticercosis with scattered calcifications has been reported; this, owing to the rarity of cases brought to our notice with certainty, is considered a medical curiosity. The case is subjected to analysis by us and we review the literature pertaining to such cases.

Aged↗
PubMedDate not supplied

Reemergence of the International Normalized Ratio for the standardization of prothrombin time.

A survey of physicians demonstrated that half had knowledge of the International Normalized Ratio (INR) but none used the value for monitoring their patients because it was not available from the Coagulation Laboratory. The Laboratory then provided the INR value at a physician's request. A six month review of prothrombin time (PT) results showed that only the physicians from the Cardiology Clinic and the Hematology Clinic employed the INR for monitoring their patients. General Medical and Surgical, Vascular, and Orthopedic Clinics continued to use the PT in seconds. This dichotomy allowed the unique opportunity to compare variability of PT in patients followed by INR and those followed by PT in seconds. Inpatients on daily monitoring were used as the standard for close control. During a six month period, laboratory reports from all patients having regular PTs and/or INRs recorded were analyzed for mean level of PT maintained, variability between individual PTs in any given patient, and instances when the PT changed > or = 5 seconds (sec) or increased to > or = 30 sec. Physicians intended to keep the PTs between 16 and 19 sec (INR 2.0 to 3.0). Results showed statistically significantly lower values of PT, less variation in values of PT and a smaller fraction of patients with changes in PT of > or = 5 sec in the group followed by INR. This group was comparable to the inpatient group but significantly different from the outpatient group followed by PT in sec.(ABSTRACT TRUNCATED AT 250 WORDS)

Drug Monitoring↗