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PURPOSE: To study if prolonged in vitro exposure to 1800MHz radiofrequency (RF) could exert an effect on human peripheral blood mononuclear cells (PBMC) from young and elderly donors by affecting apoptosis, mitochondrial membrane potential and heat shock protein (HSP) 70 levels. MATERIALS AND METHODS: Endpoints were analysed in the presence or absence of the apoptosis-inducing agent 2-deoxy-D-ribose. Three different signal modulations typical of the Global System for Mobile communication (GSM) system were applied. The modulations are widely used in mobile telephony (GSM Basic, discontinuous transmission [DTX] and Talk) at specific absorption rates of 1.4 and 2.0 W kg(-1). RESULTS: In all conditions and for all endpoints tested, there was no significant difference between RF- and sham-exposed cells. CONCLUSION: 1800MHz RF could not induce apoptosis by itself or affect the apoptotic phenomenon when induced by an apoptotic agent. Moreover, RF did not modify the mitochondrial functionality and the expression of HSP 70.

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Carboxyfullerene, a water-soluble carboxylic acid derivative of a fullerene, which acts as a free-radical scavenger, was investigated as a protective agent against ultraviolet-light-induced damage in human keratinocytes. First, we demonstrate that carboxyfullerene is not cytotoxic for these cells. In addition, this compound significantly reduces the ultraviolet-B-induced inhibition of keratinocyte proliferation and protects keratinocytes from apoptosis caused by ultraviolet B irradiation in a time- and dose-dependent fashion. Furthermore, the percentage of cells with depolarized mitochondria is significantly lower in ultraviolet-B-irradiated keratinocytes pretreated with carboxyfullerene than in cells provided with diluent alone. Carboxyfullerene also protects human keratinocytes from apoptosis induced by exposure to deoxy-D-ribose, a sugar that causes cell death through a pathway involving oxidative stress. On the other hand, ultraviolet B downregulates bcl-2 levels in human keratinocytes, and carboxyfullerene fails to prevent this effect. These results suggest that carboxy- fullerene protects human keratinocytes from ultraviolet B damage possibly via a mechanism interfering with the generation of reactive oxygen species from depolarized mitochondria without the involvement of bcl-2.

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C60 carboxyfullerene is a novel buckminsterfullerene-derived compound that behaves as a free-radical scavenger. In the present report, we investigated whether this drug exerts a protective activity against oxidative stress-induced apoptosis. Human peripheral blood mononuclear cells (PBMCs) were challenged by 2-deoxy-d-ribose (dRib) or TNF-alpha plus cycloheximide as agents that trigger apoptosis by interfering with the redox status of cell and mitochondrial membrane potential. We found that carboxyfullerene was able to protect quiescent PBMCs from apoptosis caused either by 2-deoxy-d-ribose or TNF-alpha plus cycloheximide by a mechanism partially involving the mitochondrial membrane potential integrity, known to be associated with early stages of apoptosis. These results represent the first indication for a target activity of buckminsterfullerenes on cells of the immune system and their mitochondria.

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Anoikia is a type of apoptotic cell death that occurs in cells that are substrate-restricted in their growth. Buckminsterfullerenes represent a new class of chemical compounds with wide potential pharmacological antioxidant activity. In this report we provide the first demonstration that a water-soluble fullerene derivative, C3-fullero-tris-methanodicarboxylic acid, synthesized in our laboratories, is capable of inducing anoikia resistance in epithelial cells by a mechanism involving a 'trophic' effect on cell spreading-associated cytoskeletal components, i.e. on actin microfilaments.

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The authors report six new cases of patients suffering from severe infestation with the mite sarcoptes scabiei, treated with ivermectin, currently the only oral therapy available for this disease. Each patient received 200 mug/kg of ivermectin, taken as single dose. No topical therapy was undertaken, except for topical treatment with emollient, as needed. The drug was very effective in all cases, easy to use, safe, and particularly useful in those patients with secondary eczematisation and escoriations, for whom the topical treatments are irritant and less well tolerated.

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Cardiovascular disease has a high prevalence in diabetic patients. Diabetes mellitus is an important risk factor for atherosclerosis and coronary disease mainly through obesity, hyperlipidemia, insulin-resistance, hyperinsulinemia, hyperglycemia and altered homeostasis. The correlation between diabetes and chronic heart failure is not widely documented in the literature. According to the Framingham study, the incidence of cardiovascular morbidity per year is 39.1% in diabetic males and 17.2% in diabetic females; chronic heart failure afflicts 7.6% of diabetic males and 11.4% of diabetic females. Actual knowledge about pathophysiology suggests that cardiac involvement in diabetes is not only related to macrovascular injury but also to other factors, such as alterations of autonomic nervous system, that can contribute to diabetic cardiopathy. The present study evaluated the prevalence of chronic heart failure in an Italian diabetic population in order to discuss the rationale of the therapeutic strategies.

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The response of human red blood cells (RBC) to oxidative stress has been studied with the aim to evaluate any difference in the behavior of cells from young and old subjects. Thus, RBC from 5 young (27 +/- 2 years) and 5 old (80 +/- 5 years) individuals have been treated with the organic peroxide t-butyl hydroperoxide (TBHP). The two groups behaved differently: after 4 hrs of incubation in 0.5 mM TBHP, RBC from young donors showed a higher level of hemolysis; instead, RBC from old individuals showed abnormal morphologies, being absent in unstressed RBC, with constriction and budding, which could be identified as poikilocytosis. The same abnormal forms are found in patients with spectrin mutation, leading us to hypothesize that TBHP causes damage to the cytoskeletal spectrin. This suggests that poikilocytosis might be an early stage of red blood cell hemolysis because their presence is associated to a lower level of hemolysis.

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Age-related macular degeneration (ARMD) is one of the leading causes of vision impairment in the elderly and its frequency in general population increases with aging. The etiology of this disease has remained so far unknown. The relationship between ARMD and diabetes mellitus was studied in the present work. Fundus oculi was investigated in 292 diabetic patients older than 50 years and with more than 14 years of duration of diabetes (time since diagnosis). A group of 375 non diabetic, non hypertensive subjects matched for age was studied as control. ARMD frequency was significantly higher in diabetics compared to controls (p < 0.005); and also in type II diabetics (non-insulin dependent diabetes mellitus = NIDDM) compared to type I (insulin dependent diabetes mellitus = IDDM) (p < 0.001). Older diabetic patients showed an increased frequency of ARMD while no correlation with the duration of the disease emerged. Macular damage was not linked to microangiopathy (retinopathy), hypertension or gender; on the contrary, it appeared to be associated with dyslipidemia. On the basis of these data one can conclude that diabetes mellitus can exert an unfavorable effect on macular age-related phenomena even if the pathogenetic mechanism is at present obscure.