Millimeter-wave breast cancer imaging by means of a dual-step approach combining radar and tomographic techniques: preliminary results.

Breast cancer is one of the most diagnosed forms of cancer among women worldwide. However, the survival rate is very high when the tumor is diagnosed early. The search for diagnostic techniques increasingly able to detect lesions of the order of a few millimeters and to overcome the limitations of current diagnostic techniques (e.g., the X-ray mammography, currently used as standard for screening campaigns) is always active. Among the main emerging techniques, microwave and millimeter-wave imaging systems have been proposed, using either radar or tomographic approaches. In this paper, a novel dual-step millimeter-wave imaging which combines the advantages of tomographic and radar approaches is proposed. The goal of this work is to reconstruct the dielectric profile of suspicious regions by exploiting the morphological information from the radar maps as a priori information within quantitative tomographic techniques. Promising preliminary dielectric reconstruction results against simulated data are shown in both single- and dual-target scenarios, in which high-density healthy and tumor tissues are present. The reconstruction results were compared to the dielectric characteristics of human breast exvivo tissues used in the simulated models. The proposed dual-step approach allows to distinguish the nature of the targets also in the most challenging case represented by the co-presence of high-density healthy tissues and a malignant lesion, thus paving the way for a deeper investigation of this approach in experimental scenarios. Clinical Relevance-The proposed dual-step approach in the millimeter-wave regime allows to improve the reliability of the diagnostic technique, increasing its specificity.

[Clinical evaluation of nuclear matrix protein 22 as urinary marker of transitional cell carcinoma of bladder].

OBJECTIVES. Biomarkers (BTA, NMP22, FDP etc.) have been and continue to be evaluated as adjuncts or substitutes for cystoscopy, which is invasive and uncomfortable for some patients. Nuclear matrix protein-22 (NMP22) is involved in the regulation of nuclear processes. The main objective of the present study is to evaluate the clinical utility of urinary NMP22 as a tumor marker in the follow-up of transitional cell carcinoma (TCC) of the bladder. MATERIALS AND METHODS. The study included 62 patients undergoing follow-up, who had had TCC of bladder but who were disease-free at the beginning of the study, as confirmed by cystoscopy. Urine samples were collected for urinary cytology and NMP22 test before the cystoscopy. All samples were processed according to the instructions provided with the manufacturer's kit instructions. Results. 12 cases of TCC recurrences were detected with biopsy. Cystoscopy was positive in 8 cases, NMP22 test was positive in 11 cases, and in only one case the cytopathology yielded positive results. In 14 cases NMP22 resulted as false positive. CONCLUSIONS. Urinary NMP22 appeared to be a potential tumor marker for detecting TCC of the bladder, which might rise the sensitivity of cystoscopy especially in high-grade cancer surveillance more than cytology might do.

Effect of training on H(2)O(2) release by mitochondria from rat skeletal muscle.

In this study, oxygen consumption and H(2)O(2) release rate by succinate or pyruvate/malate supplemented mitochondria isolated from skeletal muscle of trained and untrained rats were investigated. The overall mitochondrial antioxidant capacity and the effect of preincubation of mitochondria with GDP, an inhibitor of uncoupling proteins UCP1 and UCP2, on both succinate-supported H(2)O(2) release and membrane potential were also determined. The results indicate that training does not affect mitochondrial oxygen consumption with both complex-I- and complex II-linked substrates. Succinate-supported H(2)O(2) release was lower in trained than in untrained rats both in State 4 and State 3. Even the antimycin A-stimulated release was lower in trained rats. When pyruvate/malate were used as substrates, H(2)O(2) release rate was lower in trained rats only in the presence of antimycin A. The increase of mitochondrial protein content (determined by the ratio between cytochrome oxidase activities in homogenates and mitochondria) in trained muscle was such that the succinate-supported H(2)O(2) release per g of tissue was not significantly different in trained and untrained rats, while that supported by pyruvate/malate was higher in trained than in untrained animals. The lack of training-induced changes in overall antioxidant capacity of mitochondria indicates that the decrease in mitochondrial H(2)O(2) release cannot be attributed to a greater capacity of mitochondria to scavenge the reactive oxygen intermediates derived from univalent O(2) reduction by respiratory chain components. In contrast, the above decrease seems to depend on the drop induced by training in mitochondrial membrane potential. These training effects are not due to an increased level of mitochondrial uncoupling protein, because in the presence of GDP the increase in both membrane potential and H(2)O(2) release was greater in untrained than in trained rats.

Antioxidant-sensitive triiodothyronine effects on characteristics of rat liver mitochondrial population.

Whole mitochondrial population and three mitochondrial fractions were resolved by differential centrifugation from liver homogenates from euthyroid, hyperthyroid (ten daily i.p. injections of triiodothyronine (T3), 10 microg/100 g body weight) and hyperthyroid vitamin E-treated (ten daily i.m. vitamin E injections, 20 mg/100 g body weight) rats. Homogenates and mitochondrial preparations were examined for their protein content, oxidative capacity, lipid peroxidation, antioxidant status, and susceptibility to oxidative stress. In all groups, antioxidant level was smaller and oxidative capacity, lipid peroxidation, and susceptibility to oxidants were greater in the heavy mitochondrial fraction. T3 treatment was associated with increased oxidative capacity, lipid peroxidation, and susceptibility to oxidative stress, and decreased antioxidant levels in all preparations. It was also associated with increased mitochondrial protein content of homogenate and altered quantitative presence of the mitochondrial fractions. The vitamin E effects on the T3-induced changes were different for the different parameters. Vitamin E did not modify the mitochondrial protein content in liver and oxidative capacity of the various preparations, reduced the changes in both susceptibility to oxidants and contribution of each fraction to the whole mitochondrial population, and reinstated euthyroid values for antioxidant capacity and lipid peroxidation. The incomplete recovery of euthyroid resistance to oxidants in vitamin E-treated rats is due to the vitamin inability to reinstate the levels of both antioxidants and hemoproteins, on which such a resistance depends. The vitamin E effect on the composition of the mitochondrial population is more difficult to explain, because of the complexity of the mechanisms underlying the mitochondrial population modulation by thyroid hormone. However, available data suggest that such a modulation occurs through changes in the turnover of the mitochondrial fractions to which an induction of mitochondrial protein synthesis and accelerated antioxidant-sensitive degradation contribute in different measure.

Antioxidant-sensitive shortening of ventricular action potential in hyperthyroid rats is independent of lipid peroxidation.

The effects of substances able to reduce peroxidative processes on thyroid hormone-induced electrophysiological changes in ventricular muscle fibres were examined. For this study, 60 day old euthyroid and hyperthyroid rats were used. One group of hyperthyroid rats was untreated and the others were treated with vitamin E, N-acetylcysteine, and cholesterol, respectively. Hyperthyroidism was elicited by 10 day treatment with daily i.p. injections of triiodothyronine (10 microg/100 g body weight). Vitamin E and N-acetylcysteine were administered for 10 days by daily i.m. injections (20 mg/100 g body weight) and daily i.p. injections (100 mg/100 g body weight), respectively. Cholesterol was administered by cholesterol-supplemented diet (4%) from day 30. Hyperthyroidism induced a decrease in the whole antioxidant capacity and an increase in both lipid peroxidation and susceptibility to oxidative stress. Vitamin E and N-acetylcysteine administration to hyperthyroid rats led to reduction in lipid peroxidation and susceptibility to oxidative stress and to increase in antioxidant level, while the diet addition of cholesterol decreased lipid peroxidation but did not modify the other parameters. The hyperthyroid state was also associated with a decrease in the duration of the ventricular action potential recorded in vitro. The vitamin E and N-acetylcysteine administration attenuated the thyroid hormone-induced changes in action potential duration, which was however, significantly different from that of the euthyroid rats. In contrast, cholesterol supplementation did not modify the electrical activity of hyperthyroid heart. These results demonstrate that the triiodothyronine effects on ventricular electrophysiological properties are mediated, at least in part, through a membrane modification involving a free radical mechanism. Moreover, they indicate that the antioxidant-sensitive shortening of action potential duration induced by thyroid hormone is likely independent of enhanced peroxidative processes in sarcolemmal membrane.

Free radical involvement in doxorubicin-induced electrophysiological alterations in rat papillary muscle fibres.

OBJECTIVE: This work was designed to determine whether the doxorubicin-induced changes in heart electrical activity are due to increased free radical production and membrane oxidative damage. METHODS: Four groups of rats (60 days old) were used. One group was untreated and the others were treated with doxorubicin (DXR), DXR and vitamin E, and DXR and N-acetylcysteine (NAC), respectively. DXR was administered by single i.p. injection (20 mg/kg b.wt.). Vitamin E was administered by ten daily i.m. injections (100 mg/kg), while NAC (100 mg/kg) was injected i.p. 1 h before and 7 h after DXR. The effectiveness of the drug in inducing oxidative stress in different tissues and of the antioxidants in offering protection was established by determining antioxidant capacity, susceptibility to oxidative stress, and lipid peroxidation in heart, liver, and blood. The drug effect on heart electrical activity was determined by measuring the heart rate in vivo and action potential configuration in papillary muscle fibres in vitro. Heart lipid peroxidation and electrical activity were also examined in both vitamin E and NAC-treated rats. RESULTS: DXR treatment decreased antioxidant capacity and increased lipid peroxidation and susceptibility to oxidative stress in heart and blood, but not in liver. DXR administration to rats treated with antioxidants did not produce significant changes in antioxidant capacity and susceptibility to oxidative stress even in heart and blood. Furthermore, lipid peroxidation in heart and liver from DXR- and vitamin E-treated rats, and in liver from DXR- and NAC-treated rats was lower than in untreated controls. DXR treatment also increased the duration of ventricular action potentials in untreated rats, but not in antioxidant-treated rats. The treatment of control animals with the antioxidants affected lipid peroxidation, but not cardiac electrical activity. CONCLUSIONS: The protection offered by antioxidants against electrophysiological alterations indicates a free radical involvement in such alterations. In contrast, although electrical modifications are associated with increased peroxidative processes and both are prevented by the antioxidants, it is not yet clear whether a causative relationship exists between them.

Determination by enhanced luminescence technique of liver antioxidant capacity.

A simple approach to quantitative determination of antioxidant capacity of rat liver homogenate is proposed. It consists of measuring chemiluminescence generated by a suitable system "detector" for .OH radicals produced from sodium perborate. The system generating the light signal contained luminol and compounds producing enhancement of light emission, such as sodium benzoate and indophenol. Two different methods, utilizing the same technique of enhanced luminescence, were set up. In a previous work, a parameter b, contained in the equation, which best describes the dependence of the intensity of light emission (E) on liver homogenate concentration (C) (E = a.C/exp(b.C), was found to be related to the level of antioxidants in the homogenate. Therefore, in the first method, the light emission from several dilutions of both liver homogenates, and homogenate and antioxidant mixtures, stressed with sodium perborate, was detected by a luminometer. The best fitting of data to theoretical equation provided b values, which were introduced in a system of equations relating such values to the antioxidant concentration. The solution of above system supplied the antioxidant concentration in the homogenate in terms of the equivalent concentration of the antioxidant used. In the other method, evaluations of the antioxidant capacity of liver homogenates were obtained by the determination of the ability of 10% homogenates to quench the light emission induced by either peroxidase or cytochrome c in comparison to the ability of antioxidant solutions. Both methods are able to evidence the decrease of the antioxidant concentration of liver homogenates after oxidative stress with ter-butylhydroperoxide. The value of both concentration changes and standard errors indicates that the method using a standard curve obtained with peroxidase, such as catalyst of radical reaction, and deferoxamine, such as antioxidant, is to be preferred.