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Biomedical subjects

R Biondi

Publications and source records attributed to R Biondi.

45 records · Page 3Linked to original sources
PubMed1978

Reduction of testosterone to 5 alpha-dihydrotestosterone by human and rat uterine tissues.

Incubations of adult rat uterine tissue and human endometrial and myometrial homogenates with [1,2,6,7-3H]testosterone resulted in the formation of 5 alpha-[3H]dihydrotestosterone. The rat uterine homogenates showed higher activity than the minced tissue. The activity in human tissue was found to be less than rat tissue on a per unit weight basis. The human endometrium has been found to possess significantly higher activity than myometrium. These results support the hypothesis that androgens may exert their effect on uterus via 5 alpha-reduced metabolites.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1977

Regulatory mechanisms of hepatic phosphorylase in fetal and neonatal livers of rats.

Active phosphorylase was determined in rat livers during the end of the fetal period and the first days of life. This enzyme increases between the 16th day of gestation and birth. After birth, another increase in observed that takes place with 6 h. In the neonatal liver, the rapid increase in active phosphorylase, is inhibited by high levels of blood glucose, but is unaffected by actinomycin D. In fetal liver glucagon administration is followed after 5 h by an increase in total phosphorylase with only a small increase in active phosphorylase; this effect is blocked by actinomycin D. The fetal changes are interpreted as de novo synthesis, whereas the neonatal increase is due to an activation of inactive phosphorylase. Both enzymatic changes appear to be regulated by glycogen. The role of phosphorylase in the regulation of glycogen metabolism in neonatal liver is discussed.

Animals↗
PubMedDate not supplied

Neoangiogenesis in colon cancer: correlation between vascular density, vascular endothelial growth factor (VEGF) and p53 protein expression.

Angiogenesis is an essential requirement for the development, progression and metastasis of malignant tumors. Vascular endothelial growth factor (VEGF) plays an essential role in the development of angiogenesis of numerous solid malignancies, including colon cancer. The tumor suppressor gene p53 is a potent transcriptional regulator of genes which are involved in many cellular activities, including cell-cycle arrest, apoptosis and angiogenesis. In order to better understand the relation among p53 status, VEGF expression and microvessels count (MVC) in colon cancer, we evaluated immunoreactivity for CD34 endothelium-associated antigen, VEGF and p53 proteins in 43 cases of colon adenocarcinoma. Our results demonstrated an association between VEGF expression, p53 status and angiogenesis, suggesting that mutant p53 plays a central role in promoting angiogenesis in colon cancer progression.

Aged↗
PubMedDate not supplied

[Clinical significance of a carcinogenesis model of colorectal carcinoma].

OBJECTIVE: Carcinoma of the rectal colon begins as a small neoplastic polyp which gradually increases in size and, after passing through various degrees of dysplasia, develops into an overtly malignant carcinoma. Clinical experience suggests that patients may be divided into subgroups based on the aggressivity of the tumour. The genetic mutations associated with colorectal cancer have been studied and it is known that the genes primarily responsible for biological changes in the tumour cell, in the early stages, are APC, hMSH2, k-ras2 and, in particular, p53. Indeed, the mutation at the level of gene p53 has been recognized as the most common mutation in tumour cells. The aim of this study was investigate the role of p53 and CD34 in colorectal cancer. METHODS: We studied p53 positivity using immunohistological methods and compared our results with the site, stage (using the TNM system) and histological grade of the tumour. We evaluated CD34 positivity using the same methods in order to detect and quantity the presence of angiogenesis in colorectal cancer. RESULT: P53 was found to be markedly raised in the T3 stage of colorectal cancer, while its expression was decreased in stage T2 and stage T1 carcinomas and it was not detectable in adenomas. These results suggest a close correlation between the tumour stage and the expression of p53. An analogous correlation was found between CD34 expression and angiogenesis. CONCLUSION: The overexpression of p53 in epithelial cells and raised angiogenesis (as reflected in CD34 levels) in stromal cells could represent useful prognostic factors in the management of colorectal cancer.

Aged↗
PubMedDate not supplied

[The circulation of the hepatitis A and B viruses in the Somali population].

We report the results of a study carried out to evaluate the extent of hepatitis A virus (HAV) and hepatitis B virus (HBV) circulation in Somalia. Serum samples were collected from 593 subjects (age range 0-83 years) and tested for anti-hepatitis A (HAV) and anti-HAV IgM. Serum samples taken from 1272 individuals (age range 0-83 years) were tested for HBsAg, anti-HBsAg, anti-HBcAg, HBeAg and anti-HBeAg. We confirmed a very high rate of HAV exposure (about 90% of the subjects tested had circulating anti-HAV) as is typical of fecal-orally transmitted infectious agents. The age-specific anti-HAV IgM prevalence suggests that HAV infection is acquired very early in life. Our data also indicate a high rate of HBsAg carriers (range: 10.5%-27.4%) in the Somalian population. When all markers are considered, 60% of the adult population showed evidence of HBV exposure. HBV spreads very subtly: in fact, it is generally transmitted via non-overtly percutaneous routes. In Somalia, hepatitis A virus infection is highly endemic and occurs very early in life. Hepatitis B virus infection is also widespread in this country.

Age Factors↗
PubMedDate not supplied

In vitro production of leukemia inhibitory factor (LIF) by Hep G2 hepatoblastoma cells.

This study shows that the human hepatoblastoma cell line Hep G2 constitutively expressed a high level of Leukemia Inhibitory Factor (LIF) mRNA in the characteristic major 3.8 and minor 1.8 Kb forms. DNA analysis of the LIF gene from Hep G2 revealed no rearrangements. Production and secretion of significant concentrations of LIF were demonstrated by enzyme-linked immunoabsorbent assay (ELISA) in culture supernatants of Hep G2 cells. The highest LIF concentration in culture was found at 48-h (250 pg/ml). LIF produced by Hep G2 cells was biologically active since cell-free culture supernatants were able to induce in vitro differentiation of the M1 murine myeloid leukemia cell line. On the contrary, no LIF mRNA expression was detected in normal liver cells by PCR analysis. Our results suggest that LIF acts on normal parenchymal hepatocytes through a paracrine mechanism and on Hep G2 cells by an autocrine action. Furthermore they indicate that the Hep G2 cell line could be an useful model for studying the LIF autocrine mechanism in hepatomas.

Base Sequence↗