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A Pola

Publications and source records attributed to A Pola.

15 recordsLinked to original sources

A solid state microdosimeter based on a monolithic silicon telescope.

A monolithic silicon telescope, consisting of a DeltaE and an E stage-detector ( approximately 1.9 microm and 500 microm thick, respectively), was coupled to a polyethylene converter in order to investigate the feasibility of a solid state microdosimeter with respect to the field-funnelling effect. This work discusses the preliminary results of an analytical approach for the correction of a spectrum measured with this silicon-based microdosimeter for tissue-equivalence and geometrical effects. The device was irradiated with 2.7 MeV monoenergetic neutrons at the INFN-Laboratori Nazionali di Legnaro (Legnaro, Italy). The non tissue-equivalence of silicon was corrected by exploiting the signals generated in the E-stage. The correction for the sensitive volume geometry was optimised by taking into account the track length distribution of the recoil-protons generated in the converter. The derived dose distribution of the energy imparted per event was compared to the one measured with a cylindrical tissue-equivalent proportional counter (TEPC). The agreement is satisfactory.

Computer-Aided Design↗

A feasibility study of a solid-state microdosimeter.

A solid-state silicon detector is a challenging device for microdosimetry, mainly because it can provide sensitive zones of the order of a micrometer. Moreover, these detectors are characterized by a high spatial and a good energy resolution. However, they may present some limitations, such as: (i) the minimum detectable energy which is limited by the electronic noise; (ii) radiation hardness; (iii) the geometry of the sensitive volume; (iv) the field-funnelling effect; (v) the non-tissue-equivalence of silicon. This work discusses a feasibility study of a microdosimeter based on a monolithic silicon telescope, consisting of a DeltaE and an E stage-detector, about 1 and 500 microm thick, respectively. Charges are collected separately in the two stage-detectors. The use of the DeltaE stage coupled with a tissue-equivalent converter was investigated as a solid-state microdosimeter. Irradiations with monoenergetic neutrons were performed at the INFN-Laboratori Nazionali di Legnaro (Italy). The field-funnelling effect appears to be negligible from the comparison of the experimental data with the results of Monte Carlo simulations, performed with the FLUKA code. The preliminary results of an analytical approach for the correction for geometrical effects and tissue-equivalence are also presented.

Journal Article↗

Performance of a neutron spectrometer based on a PIN diode.

The neutron spectrometer discussed in this work consists of a PIN diode coupled with a polyethylene converter. Neutrons are detected through the energy deposited by recoil-protons in silicon. The maximum detectable energy is -6 MeV and is imposed by the thickness of the fully depleted layer (300 microm for the present device). The minimum detectable energy which can be assessed with pulse-shape discrimination (PSD) is -0.9 MeV. PSD is performed with a crossover method and setting the diode in the 'reverse-injection' configuration (i.e. with the N+ layer adjacent to the converter). This configuration provides longer collection times for the electron-hole pairs generated by the recoil-protons. The limited interval of detectable energies restricts the application of this spectrometer to low-energy neutron fields, such as the ones which can be produced at facilities hosting low-energy ion accelerators. The capacity to reproduce continuous neutron spectra was investigated by optimising the electronic chain for pulse-shape discrimination. In particular, the spectrometer was irradiated with neutrons that were generated by striking a thick beryllium target with protons of several energies and the measured spectra were compared with data taken from the literature.

Equipment Design↗

Secondary photon fields produced in accelerator-based sources for neutron generation.

Neutrons can be produced with low-energy ion accelerators for many applications, such as the characterisation of neutron detectors, the irradiation of biological samples and the study of the radiation damage in electronic devices. Moreover, accelerator-based neutron sources are under development for boron neutron capture therapy (BNCT). Thin targets are used for generating monoenergetic neutrons, while thick targets are usually employed for producing more intense neutron fields. The associated photon field produced by the target nuclei may have a strong influence on the application under study. For instance, these photons can play a fundamental role in the design of an accelerator-based neutron source for BNCT. This work focuses on the measurement of the photon field associated with neutrons that are produced by 4.0-6.8 MeV protons striking both a thin 7LiF target (for generating monoenergetic neutrons) and a thick beryllium target. In both cases, very intense photon fields are generated with energy distribution extending up to several MeV.

Beryllium↗

A recoil-proton spectrometer based on a p-i-n diode implementing pulse-shape discrimination.

A recoil-proton spectrometer was created by coupling a p-i-n diode with a polyethylene converter. The maximum detectable energy, imposed by the thickness of the totally depleted layer, is approximately 6 MeV. The minimum detectable energy is limited by the contribution of secondary electrons generated by photons in the detector assembly. This limit is approximately 1.5 MeV at full-depletion voltage and was decreased using pulse-shape discrimination. The diode was set up in the 'reverse-injection' configuration (i.e. with the N+ layer adjacent to the converter). This configuration provides longer collection times for the electron-hole pairs generated by the recoil-protons. The pulse-shape discrimination was based on the zero-crossing time of bipolar signals from a (CR)2-(RC)2 filter. The detector was characterised using monoenergetic neutrons generated in the Van De Graaff CN accelerator at the INFN-Laboratori Nazionali di Legnaro. The energy limit for discrimination proved to be approximately 900 keV.

Body Burden↗

Direct effect of the correction of acidosis on plasma parathyroid hormone concentrations, calcium and phosphate in hemodialysis patients: a prospective study.

BACKGROUND: Metabolic acidosis contributes to renal osteodystrophy and together with hyperphosphatemia, hypocalcemia and altered vitamin D metabolism may result in increased levels of intact parathyroid hormone (iPTH) and metastatic calcifications. However, the impact of the correction of metabolic acidosis on iPTH levels and calcium-phosphate metabolism is still controversial. STUDY DESIGN: The effects of the correction of metabolic acidosis on serum concentrations of iPTH, calcium (Ca), phosphate (PO(4)) and alkaline phosphatase were prospectively studied. Twelve uremic patients on maintenance hemodialysis (HD) for 49 months (median; range 6-243 months) with serum bicarbonate levels < or =20 mmol/l were studied before and after 3 months of oral sodium bicarbonate supplementation. Predialysis serum bicarbonate, arterial pH, ionized calcium, plasma sodium, plasma potassium, serum creatinine, hemoglobin, K(t)/V, postdialysis body weight, predialysis systolic and diastolic blood pressure were also evaluated before and after correction. RESULTS: Serum bicarbonate levels and arterial pH increased respectively from 19.3 +/- 0.6 to 24.4 +/- 1.2 mmol/l (p < 0.0001) and 7.34 +/- 0.03 to 7.40 +/- 0.02 (p < 0.001). iPTH levels decreased significantly from 399 +/- 475 to 305 +/- 353 pg/ml (p = 0.026). No changes in total serum Ca, plasma PO(4), serum akaline phosphatase, K(t)/V, serum creatinine, hemoglobin, body weight, predialysis systolic and diastolic blood pressures were observed. iCa decreased significantly. CONCLUSIONS: Our study demonstrates that the correction of metabolic acidosis in chronic HD patients reduces iPTH concentrations in HD patients with secondary hyperparathyroidism possibly by a direct effect on iPTH secretion.

Acid-Base Equilibrium↗

Cholesterol crystal embolism: A recognizable cause of renal disease.

Cholesterol crystal embolism, sometimes separately designated atheroembolism, is an increasing and still underdiagnosed cause of renal dysfunction antemortem in elderly patients. Renal cholesterol crystal embolization, also known as atheroembolic renal disease, is caused by showers of cholesterol crystals from an atherosclerotic aorta that occlude small renal arteries. Although cholesterol crystal embolization can occur spontaneously, it is increasingly recognized as an iatrogenic complication from an invasive vascular procedure, such as manipulation of the aorta during angiography or vascular surgery, and after anticoagulant and fibrinolytic therapy. Cholesterol crystal embolism may give rise to different degrees of renal impairment. Some patients show only a moderate loss of renal function; in others, severe renal failure requiring dialysis ensues. An acute scenario with abrupt and sudden onset of renal failure may be observed. More frequently, a progressive loss of renal function occurs over weeks. A third clinical form of renal atheroemboli has been described, presenting as chronic, stable, and asymptomatic renal insufficiency. The renal outcome may be variable; some patients deteriorate or remain on dialysis, some improve, and some remain with chronic renal impairment. In addition to the kidneys, atheroembolization may involve the skin, gastrointestinal system, and central nervous system. Renal atheroembolic disease is a difficult and controversial diagnosis for the protean extrarenal manifestations of the disease. In the past, the diagnosis was often made postmortem. However, in the last decade, awareness of atheroembolic renal disease has improved, enabling us to make a correct premortem diagnosis in a number of patients. Correct diagnosis requires the clinician to be alert to the possibility. The typical patient is a white man aged older than 60 years with a baseline history of hypertension, smoking, and arterial disease. The presence of a classic triad characterized by a precipitating event, acute or subacute renal failure, and peripheral cholesterol crystal embolization strongly suggests the diagnosis. The confirmatory diagnosis can be made by means of biopsy of the target organs, including kidneys, skin, and the gastrointestinal system. Thus, Cinderella and her shoe now can be well matched during life. Patients with renal atheroemboli have a dismal outlook. A specific treatment is lacking. However, it is an important diagnosis to make because it may save the patient from inappropriate treatment. Finally, recent data suggest that an aggressive therapeutic approach with patient-tailored supportive measures may be associated with a favorable clinical outcome.

Adult↗

Correction of metabolic acidosis increases serum albumin concentrations and decreases kinetically evaluated protein intake in haemodialysis patients: a prospective study.

BACKGROUND: Metabolic acidosis in haemodialysis (HD) patients increases whole body protein degradation while the correction of acidosis reduces it. However, the effects of the correction of acidosis on nutrition have not been clearly demonstrated. STUDY DESIGN: In this study we have evaluated the effects of 3 months of correction of metabolic acidosis by oral sodium bicarbonate supplementation on protein catabolic rate (PCRn) and serum albumin concentrations in 12 uraemic patients on maintenance HD for at least 6 months (median 49 months; range 6-243 months). Pre-dialysis serum bicarbonate, arterial pH, serum albumin, total serum proteins, serum creatinine, plasma sodium, haemoglobin, PCRn, Kt/V, and TACurea, were evaluated before and after correction. RESULTS: Serum bicarbonate levels and arterial pH increased respectively from 19.3 +/- 0.6 mmol/l to 24.4 +/- 1.2 mmol/l (P < 0.0001) and 7.34 +/- 0.03 to 7.40 +/- 0.02 (P < 0.0001). Serum albumin increased from 34.9 +/- 2.1 g/l to 37.9 +/- 2.9 g/l (P < 0.01), while PCRn decreased from 1.11 +/- 0.17 g/kg/day to 1.03 +/- 0.17 g/kg/day (P < 0.001). No changes in Kt/V, total serum proteins, serum creatinine, plasma sodium, haemoglobin, body weight, pre dialysis systolic and diastolic blood pressure, and intradialytic weight loss were observed. CONCLUSIONS: Our data demonstrate that correction of metabolic acidosis improves serum albumin concentrations in HD patients. The correction of acidosis induces a decrease in PCRn values, as evaluated by kinetic criteria, suggesting that in the presence of moderate to severe acidosis this parameter does not reflect the real dietary protein intake of the patients probably as a result of increased catabolism of endogenous proteins. The correction of metabolic acidosis should be considered of paramount importance in HD patients.

Acidosis↗

Predictive value of dialysis adequacy and nutritional indices for mortality and morbidity in CAPD and HD patients. A longitudinal study.

BACKGROUND: The effects of dialysis inadequacy on patient survival and nutritional status and that of malnutrition on survival have not been clearly assessed. Studies comparing dose/mortality and morbidity curves on continuous ambulatory peritoneal dialysis (CAPD) and on haemodialysis (HD) are also needed, to assess adequate treatment on CAPD. METHODS: We have evaluated the effects of age, 13 pretreatment risk factors, serum albumin, transferrin, normalized protein catabolic rate, Kt/V, normalized weekly creatinine clearance, residual renal function and subjective global assessment of nutritional status on survival and morbidity, in a 3-year prospective study of 68 CAPD and 34 HD patients. RESULTS: Survivals did not differ for CAPD and HD patients. In the Cox hazard regression model, age, peripheral vasculopathy, serum albumin < 3.5 g/dl and Kt/V < 1.0/treatment on HD and < 1.7/week on CAPD were independent factors negatively affecting survival. On the contrary, adjusted survivals were not affected by gender, modality, other comorbid factors, normalized protein catabolic rate, or subjective global assessment of nutritional status. Persistence of residual renal function significantly improved survival. Observed and adjusted survival did not significantly differ for CAPD and HD patients with either low (HD, < 1.0/treatment; CAPD, < 1.7/week) or high ( > or = 1.0 and > or = 1.7) Kt/V. On HD, adjusted survivals were similar for 1.0 < or = Kt/V < 1.2 or > or = 1.2. On CAPD, Kt/V > or = 1.96/week was associated with definitely better survival, with only one death/23 patients versus 19/45, with Kt/V < or = 1.96. Survival was not different for 1.96 < or = Kt/V < 2.03 and > or = 2.03. Normalized weekly creatinine clearance and wKt/V were positively related on CAPD (r 0.39, P < 0.01) and wKt/V = 1.96 corresponded to 58 litres of normalized weekly creatinine clearance. CONCLUSIONS: Indices of adequacy were predictors of mortality and morbidity, both on CAPD and HD, whereas normalized protein catabolic rate and subjective global assessment of nutritional status were not. Serum albumin did not decrease during dialysis; hence its predictive effect for survival is due to the predialysis condition and not to dialysis-induced malnutrition.

Adult↗

Clinical and biochemical responses to therapy in Alzheimer's disease and multi-infarct dementia.

Memory performance, central monoaminergic function and sympathetic nerve activity were studied in patients with dementia of the Alzheimer type (DAT) or with multi-infarct dementia before and after 4 weeks with single or combined drug therapy (choline-piracetam). Analysis of the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG), 3-methoxy-4-hydroxyphenylacetic acid (HVA) and 5-hydroxyindolacetic acid in the cerebrospinal fluid (CSF) and also in urine (plus 3-methoxy-4-hydroxy mandelic acid) showed that the basal values of HVA in the CSF and urine were lower in the more severely demented compared with the mildly demented subjects in both groups. The combined drug treatment resulted in a statistically significant increase in the MHPG level in the CSF of mildly demented subjects of the DAT group, while it seemed not to influence the other monoamine metabolites. The sympathetic nerve activity was similar in both patient groups and was unchanged after therapy. These findings suggest a dopaminergic deficit in advanced stages of the disease and a possible enhancement of the central noradrenergic output with therapy. No effects of therapy on memory performance or correlations between monoamine levels and memory test scores were noted.

Aged↗