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Biomedical subjects

A Magrini

Publications and source records attributed to A Magrini.

62 records · Page 4Linked to original sources

[Noise-induced hearing loss: new preventive approaches].

Noise-induced hearing loss is currently the most frequent professional disease in Italy. Genetic polymorphisms of genes involved in the pathophysiology of hearing loss may confer vulnerability to the damage. To obtain data on these polymorphisms able to make a single worker more susceptible or resistant than others to the damage of the organ of Corti after exposure to noise, may allow a more efficient prevention.

Hearing Loss, Noise-Induced↗

[Water perception and utilization in a sample of students in the province of Viterbo].

Nowadays water quality is certainly one of the issues of major concern. Control on waterway considerably involves public hygiene services and represents a prevention activity and a measure of public health safety, which often is unknown to the population. For this reason the Public Hygiene Service of Viterbo L.H.U. (Local Health Unit) in collaboration with the Institute of Hygiene of the Catholic University of Rome carried out a survey to evaluate perception towards tap water quality in a sample of students. During the last decade tap and mineral water consumption habits turned out to be constant. The great majority of students reported to use widely mineral water at home; mineral water consumption was high regardless of social class. Since our investigation found a large use of mineral water in this town, the L.H.U. could intervene to modify these attitudes, starting up with an education campaign of the population: tap water is indeed subject to quality controls with a higher frequency compared to mineral water.

Adolescent↗

[Lack of direct cytotoxic effect of intracellular nanotubes].

Nanotubes have a great therapeutic potential due to their astounding physico-chemical features, the possibility to be funtionalised for ad hoc uses, and the specific interaction of nanotubes as such with life molecules (DNA and proteins). These features recommend a thorough toxicological study before widespread pharmaceutic use. We provide evidence that culture cells with phagocytic potential internalise multi wall nanotubes (10-50 nm average size). This is not accompanied by cytotoxicity in terms of induction of &apoptosis or necrosis at the doses used (up to 125 microg/mI).

Apoptosis↗

[Carbon nanotubes (CNT) and nanoparticles (NP): interaction with lung epithelium and other biological systems].

Carbon nanotubes (CNT) and nanoparticles (NP) represent new classes of technological materials with innovative properties. Although inhalation is less likely for engineered nanomaterials (NM) compared with ambient or mineral dust particles, this can happen during bulk manufacture and handling of freely dispersable NP at workplace. Both environmental and engineered NP are able to cause oxidative stress, reactive oxygen species (ROS) generation, NF-kappaB activation, but some of the possible NM interactions with biological systems may result in additional forms of injury. NP can impair fagocytosis, can enhance macrophage sensitivity to chemotactic factors (MCP-1), thus worsening antigen-mediated inflammation. Metal NP (e.g. TiO2, Al2O3 and Fe3O4) can impair mitochondrial function, leading to a dramatic reduction of the intracellular glutathione pool, thus compromising cell viability and morphology. CNTs are a man-made form of crystalline carbon currently attracting intense research efforts because of their unique properties, that make them suitable for many uses in biomedicine and pharmacology. CNTs stimulate TNF-alpha production in the lung, inducing inflammatory reactions, but they can also cross cell membranes reacting with DNA and aminoacidic residues, leading to cell apoptosis. Larger CNTs could have features of conventional fibers and show the ability to stimulate mesenchymal cell growth and to cause lung granulomas formation and fibrotic reactions. These results suggest that NM are potentially hazardous to humans and that strict industrial hygiene measures should be taken to limit exposure during their manipulation.

Humans↗

Mild brain ischemia increases cerebral lipid peroxidation and activates leukocytes in the peripheral blood of rats.

This study evaluated local and systemic leukocyte changes, respectively in the jugular and femoral veins, after an acute reduction of cerebral blood flow (oligoemia) in rats submitted either to permanent bilateral carotid occlusion (BCO) (no. = 36) for 5 hours or to sham operation (no. = 33). In a subgroup of rats (no. = 13) the extent of neural damage was histologically assessed. As a marker of biochemical brain changes the entity of the iron-ascorbate induced lipid peroxidation of synaptosomes was assessed in vitro by measuring malondialdehyde (MDA) reactive products. Five hours after surgery, the percentage of aggregated leukocytes and of activated neutrophils reducing the NBT were significantly higher in BCO rats (p < 0.05). However, leukocyte changes did not differ significantly between the jugular and the femoral districts. The brains of BCO rats showed tiny foci of neuronal necrosis. Synaptosomes obtained from the BCO animals showed a small but highly significant increase of MDA production (p < 0.01). Long-lasting brain oligoemia increases the production of lipid peroxidative metabolites, and causes the occurrence of tiny foci of neuronal necrosis in different brain regions. The lack of a significant gradient in aggregated leukocytes and activated neutrophils between the jugular and femoral venous districts demonstrates that leukocytes are stimulated in the peripheral blood by even mild biochemical and morphological brain damage.

Animals↗