Biomedical subjects

E Benetti

Publications and source records attributed to E Benetti.

6 recordsLinked to original sources

PubMed2006

Clinical and molecular markers of chronic interstitial nephropathy in congenital unilateral ureteropelvic junction obstruction.

PURPOSE: We evaluated clinical and biological variables, and their meaning as reliable markers of chronic interstitial nephropathy in a selected group of children with prenatally detected hydronephrosis who underwent pyeloplasty because of congenital unilateral ureteropelvic junction obstruction. MATERIALS AND METHODS: We reviewed the clinical, prenatal and postnatal ultrasonographic, and scintigraphic records of children for whom intraoperative biopsy records were available. We performed histological analysis, and evaluated tubulointerstitial immunostaining for vimentin and alpha-smooth muscle actin, and the immunohistochemical and mRNA expression of the renin-angiotensin system peptides and transforming growth factor-beta1. RESULTS: The children were divided in 2 groups according to the absence (group 1) or presence (group 2) of chronic interstitial nephropathy in the biopsy. Patients in group 2 were significantly younger at prenatal diagnosis (p = 0.031), and had decreased split renal function (p = 0.005) and worse drainage (p = 0.035) on preoperative diuretic renography. No differences were found in terms of degree of hydronephrosis, or its prenatal and postnatal variation. Group 2 biopsies exhibited greater immunostaining for alpha-smooth muscle actin and vimentin (p = 0.004 and p = 0.047, respectively), and transforming growth factor-beta1 mRNA levels (p = 0.06). Vimentin and alpha-smooth muscle actin positivity correlated with renin, angiotensin II receptors 1 and 2, and transforming growth factor-beta1 mRNA levels, and all correlated with preoperative split renal function and post-void washout. CONCLUSIONS: In congenital unilateral ureteropelvic junction obstruction chronic interstitial nephropathy and poor postoperative recovery seem to be associated with an earlier diagnosis of hydronephrosis, functional loss greater than 10% and worse scintigraphic drainage. Moreover, there is a strong correlation between molecular fibrogenic markers and histologically and scintigraphically demonstrated renal damage.

Actins↗

PubMed2004

Kinetics of surfactant in respiratory diseases of the newborn infant.

Deficiency or dysfunction of pulmonary surfactant plays a critical role in the pathogenesis of respiratory diseases in the newborn. We describe the studies made by applying two recently developed methods to measure surfactant kinetics. The first allows the measurement of endogenous surfactant phosphatidylcholine (PC) synthesis and kinetics by a constant intravenous infusion of glucose or fatty acids labeled with stable isotope 13C. The second method consists of endotracheal administration of a tracer dose of 13C-labeled dipalmitoyl-phosphatidylcholine (DPPC) to measure disaturated-phosphatidylcholine (DSPC) half-life and apparent pool size. We present the results of surfactant kinetics in some of the respiratory diseases of the newborn infant.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1988

Radionuclide evaluation of lung perfusion after the Fontan procedure.

Lung perfusion was evaluated in 19 patients in whom a Fontan operation had been performed at a mean age of 3.7 years. First pass and equilibrium data were acquired during the lung particle perfusion scan 0.5 to 7.9 years (mean 3.7 years) following the Fontan procedure. Abnormalities of lung perfusion were documented in 8 patients. Minimal underperfusion of small areas of either right or left lung were noted in 4 patients, while the remaining 4 had evidence of major perfusion defects, involving both lungs. The perfusion defects were localized, in the majority of cases, on the side where a palliative procedure had been performed before the Fontan operation: it is of note that all our patients without palliative procedures did not show abnormalities in lung perfusion. Major abnormalities of lung perfusion seemed related to possible intimal thrombosis or emboli due to prolonged polycythemia or to pulmonary vessel distortion due to long-standing shunts.

Child↗

PubMed1988

Charcot-Marie-Tooth disease and cardiac arrhythmias.

A child with several episodes of supraventricular tachycardia was treated in our department from birth to the age of seven years. At this age a diagnosis of Charcot-Marie Tooth disease was made on the basis of the results of clinical and neurophysiological examinations, blood analysis and a neuromuscular biopsy. The association between sensorimotor neuropathies and cardiac involvement is controversial, especially at pediatric ages. We describe a case presenting this association.

Charcot-Marie-Tooth Disease↗

PubMed1986

Plasma zinc levels in children with chronic diarrhoea.

We measured the plasma zinc concentration in a group of children with chronic diarrhoea. Fifteen patients with untreated coeliac disease had a mean plasma zinc level significantly lower than that of healthy children (69 micrograms/dl vs 96 micrograms/dl). In patients with chronic post-enteritic diarrhoea (n = 70) the mean plasma zinc level was in the normal range (100 micrograms/dl). The latter result suggests that our country a secondary zinc deficiency is not a feature of chronic post-enteritic diarrhoea.

Celiac Disease↗

PubMedDate not supplied

[Syncope in childhood].

Syncope may be defined a sudden and transient loss of consciousness due to a reversible alteration of brain function. Three main groups of syncopes can be identified: cardiac, vascular and non-cardiovascular. All the patients (63) admitted to the emergency unit of Pediatric Clinic of the University of Padua from January 83 to July 84 and reporting one or more episodes of loss of consciousness were examined. Their age ranged from 1 month to 15 years. All the patients were investigated with the same study protocol: ECG, EEG, 24 hours ECG monitoring, routine blood examinations; other tests were done when needed. The cause of syncope was established in 53,8% of cases; for 6,3% of patients the cause was cardiac (arrhythmic), in 38% it was vascular (vasovagal syncope), in 6,3% it was non-cardiovascular (neurologic or metabolic). The cause of syncope was not identified in 46% of the patients, which is also in agreement with other studies. However, we were able, through the use of our protocol, to identify quickly and non invasively the etiology of the syncope in 25% of the patients.

Adolescent↗