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Biomedical subjects

A Benedetti

Publications and source records attributed to A Benedetti.

At least 145 records · Page 8Linked to original sources
PubMed1990

Immunohistochemical identification of proliferating cells following dimethylnitrosamine-induced liver injury.

The present study is concerned with changes in the number and localization of S-phase cells in the liver of rats exposed to dimethylnitrosamine (DMN). S-phase cells were detected by immunohistochemistry after injection of bromodeoxyuridine (BrdU) and exposure of paraffin sections of liver tissue to the antibody anti-BrdU. With respect to controls, the number of S-phase cells increased four to fivefold in DMN-treated animals in the first week of treatment and remained significantly higher thereafter, in association with the formation of septa. At all times, the labelling index was higher in littoral cells than in hepatocytes. No labelling was observed in biliary cells. This behaviour is different from that reported in other situations, for instance in regeneration after partial hepatectomy, which suggests that besides hepatocytes and littoral cells replacement, an involvement of the latter cell line in the inflammatory reaction, synthesis of extracellular matrix components and formation of septa may account for this particular pattern.

Animals↗
PubMed1990

Linear accelerator radiosurgery of three-dimensional irregular targets.

Current radiosurgical techniques allow concentration of radiation from external sources into spherical targets. Nonspherical target volumes require a modification of the irradiation technique. Moreover, isodose shaping is sometimes necessary to spare nearby important radiosensitive structures. To meet these prerequisites we have introduced some technical refinements: (1) computer-controlled rectilinear translations of the target in combination with different angular positions of the source and (2) computer-controlled rotations of the target around a vertical axis in combination with different angular positions of the source. The first solution has proven efficient for treating irregular targets, while the second one was employed for focusing the radiation dose inside volumes obtained by rotation of ellipses.

Brain Neoplasms↗
PubMed1990

Multimarker immunohistochemical staining of calgranulins, chloroacetate esterase, and S100 for simultaneous demonstration of inflammatory cells on paraffin sections.

Mac387 monoclonal antibody (MAb) recognizes two calcium binding, myeloid-associated proteins, now termed calgranulins, expressed at high levels by neutrophils and monocytes. Calgranulins are related to migration inhibitory factor (MIF) and are lost in a few days from monocytes differentiated in vitro. This marker is therefore potentially useful to analyze macrophage heterogeneity and turnover in tissue sections. In this study, we developed an immunohistochemical multimarker technique, including calgranulin demonstration, suitable for analyzing different inflammatory cells on paraffin-embedded material. The technique was carried out in subsequent steps demonstrating (a) naphthol AS-D chloroacetate esterase (CAE); (b) S100 immunoreactivity using a rabbit antibody in peroxidase-antiperoxidase (PAP) staining; and (c) Mac387 immunoreactivity using the alkaline phosphatase-anti-alkaline phosphatase (APAAP) technique. CAE staining was introduced in this method to distinguish Mac387+/CAE- macrophages from Mac387+/CAE+ neutrophils, and Mac387-/CAE+ mast cells. S100 protein is strongly expressed within lymphoid tissues by dendritic accessory cells and was then applied to distinguish these cells from S100-macrophages. We have also verified the possibility of reducing the staining time for this time-consuming procedure by use of microwave irradiation. The technique was applied to a representative variety of normal and pathological samples to assess its usefulness for study of cell heterogeneity. Our results showed the multimarker technique to be highly informative in the study of inflammatory lesions (e.g., rheumatoid arthritis, sarcoid and cat-scratch granulomas, dermathopathic lymphadenopathy), and is of wide potential value as an aid to histopathological diagnosis of several diseases.

Antibodies, Monoclonal↗
PubMed1990

On the role of lipid peroxidation and protein-bound aldehydes in the haloalkane-induced inactivation of microsomal glucose 6 phosphatase.

The inactivation of liver microsomal glucose 6 phosphatase induced either by Fe2+ or by haloalkanes (CCl4, CBrCl3) was investigated in NADPH-microsomes systems. In the case of haloalkanes, EDTA was included in the incubation mixtures, so to exclude participation of free Fe2+ in the ensuing lipid peroxidation. Microsomal glucose 6 phosphatase activity was measured along with the release of malonic dialdehyde and the appearance of carbonyl products bound to microsomal protein, taken as indices of the peroxidative process. Fe2+ was added to NADPH-microsomes at different concentrations, one (6 microM) resulting in an extent of lipid peroxidation comparable with that induced by haloalkanes, the other (60 microM) representing a situation of excess Fe2+, leading to massive lipid peroxidation. Inhibition of glucose 6 phosphatase caused by 6 microM Fe2+ was comparable to that induced by haloalkanes in EDTA-microsomes systems, which supports the view that lipid peroxidation--rather than covalent binding of free radical metabolites--represents the main event leading to the inactivation of glucose 6 phosphatase caused by haloalkanes. The production of 4-hydroxynonenal--the known toxic product of lipid peroxidation--was also studied. A remarkable accumulation of 4-hydroxynonenal was observed in the microsomal membranes after peroxidation induced by 6 microM Fe2+ or haloalkanes, as compared to the incubation medium. In addition, experiments carried out with CCl4 and CBrCl3 in vivo suggested the possible existence of a cytosolic detoxification system able to remove lipid-derived carbonyls bound to microsomal protein.

Aldehydes↗
PubMed1990

Intra-operative monitoring by means of somatosensory evoked potentials during cerebral aneurysms surgery.

During cerebral aneurysms surgery, brain tissue may suffer for global or local ischemia due to deliberate hypotension and surgical manoeuvres. Somatosensory evoked potentials (SEPs) can detect functional derangements consequent to hypoxia, before a permanent brain damage is produced. Forty two patients, undergoing cerebral aneurysms surgery for treatment of SAH, were evaluated intraoperatively with SEP recordings. It has been stressed that no permanent neurological damage is to be expected if the absolute value of Central Conduction Time (CCT) does not exceed 9.5 ms for 10 min at least and the cortical waves are visible throughout the whole procedure. SEP changes are strictly related with MAP decrease and surgical handlings.

Adult↗
PubMed1990

The transcranial Doppler ultrasonography in the evaluation of vasospasm and of intracranial hypertension after subarachnoid hemorrhage.

The transcranial doppler (T.C.D.) is a non-invasive technique useful for the evaluation of vasospasm and intracranial hypertension in patients with subarachnoid hemorrhage (S.A.H.). Eighteen patients with recent S.A.H. were studied by means of T.C.D. device: in 14 patients the source of bleeding was a ruptured aneurysm of the circle of Willis, while the remaining 4 presented a negative four-vessels angiography. All the patients were studied 5 and 10 days after the bleeding. Our data showed that the ultrasonographic demonstration of vasospasm and/or I.C.H. is clearly related to the clinical status of the patients. No significant T.C.D. difference was noticed between the "sine materia" S.A.H. patients and the ones with ruptured aneurysm.

Blood Flow Velocity↗
PubMed1989

Liver cytosolic non-dialysable factor(s) can counteract GTP-dependent Ca2+ release in rat liver microsomal fractions.

Readdition to rat liver microsomes of dialysed liver post-microsomal supernatant resulted in an almost complete inhibition of the Ca2+-releasing effect of GTP. Such inhibition was heat-labile, and was associated with non-ultrafiltrable supernatant components with a molecular weight higher than 30,000 D. A preliminary fractionation of liver supernatant showed that the inhibitory effect is recovered in the 40-50% ammonium sulfate-precipitated proteins, with an approx. 10-fold enrichment. The active ammonium sulfate fraction did not modify the GTP-induced Ca2+ increase of passive Ca2+ efflux from microsomes, nor did it affect microsomal GTP hydrolysis, which is likely required for its Ca2+ releasing effect. The active ammonium sulfate fraction appears to markedly favour the translocation of GTP-released Ca2+ into a microsomal GTP-insensitive pool. Separation of liver microsomes in smooth and rough fractions revealed that such GTP-insensitive Ca2+ pool is almost completely associated with smooth microsomes.

Animals↗
PubMed1989

Ca2+ mobilization by vasopressin and glucagon in perfused livers. Effect of prior intoxication with bromotrichloromethane.

Perfused livers isolated from rats treated with BrCCl3 for up to 15 min were used as an experimental tool to investigate the role of the hepatic endoplasmic reticulum in Ca2+ mobilization elicited by vasopressin and glucagon. BrCCl3-treatment caused extensive impairment (37 to 92%) of Ca2+ pumps of isolated liver microsomes, while Ca2+ pumps of mitochondria and plasma membrane vesicles remained undamaged. In perfused livers of BrCCl3-treated rats, the efflux of Ca2+ and the concomitant stimulation of O2 consumption and glucose release induced by vasopressin were decreased. The extent of the decrease paralleled the duration of BrCCl3-treatment. The decrease of Ca2+ efflux following vasopressin addition was closely correlated with the decrease of active Ca2+ accumulation by isolated microsomes (r = 0.99, P less than 0.001). The Ca2+ efflux elicited by glucagon was also decreased after BrCCl3-treatment, whereas stimulation of O2 consumption and glucose release were retained. The possibility that BrCCl3-treatment might impair the production of the intracellular Ca2+-mobilizing messenger IP3 is unlikely, since vasopressin still induced the formation of inositol phosphates, including IP3, in isolated hepatocytes obtained from BrCCl3-treated rats. Thus, this work supports the hypothesis that the Ca2+ stored in the liver ER is the major pool of intracellular Ca2+ available for mobilization by vasopressin, glucagon and other effectors.

Animals↗
PubMed1989

Low-grade astrocytomas: treatment with unconventionally fractionated external beam stereotactic radiation therapy.

Fourteen patients with nonoperable low-grade astrocytomas were treated with unconventionally fractionated stereotactic radiation therapy. The target volume was defined with computed tomography (CT) performed under stereotactic conditions. The treatment was carried out with a technique producing multiple noncoplanar arc irradiation, with the center of the target volume placed at the isocenter of the linear accelerator. A total dose of 16-50 Gy was administered in either one fraction or two fractions 8 days apart. The concentration of dose within the target volume allowed reduction of dose absorbed by adjacent critical structures of the intact brain. Patients were followed up for 11-48 months. Twelve of 14 patients had a partial or complete response to treatment, as demonstrated by CT. Stereotactic radiation therapy appears to be effective in the control of small radioresistant cerebral neoplasms, without damaging surrounding healthy tissues.

Adolescent↗
PubMed1989

Linear accelerator radiosurgery of cerebral arteriovenous malformations.

A technique for linear accelerator radiosurgery has been used in clinical practice since 1982. The technique is based on multiple intersecting arc irradiations focused on a stereotactic target. From November 1984 to October 1988, 97 patients with cerebral arteriovenous malformations have been treated. Seventy-nine patients suffered one or more than one hemorrhage. Four patients had progressive neurological symptoms. In 14 patients, epilepsy was the principal complaint. Stereotactic localization was performed by stereotactic angiography. Lesion dimensions varied from 4 to 40 mm in diameter. Doses from 18.7 to 40 Gy were delivered in one or two sessions. Mean follow-up is 17.1 months (from 1 to 49). Four instances of minor rebleeding were observed after treatment; 3 patients complained of transient neurological deterioration. Of 56 patients who were followed longer than 1 year, 50 underwent 12-month follow-up angiography. In 26 patients complete obliteration of the malformation was demonstrated (52%), in 12 patients subtotal obliteration was obtained (24%), in 11 patients the obliteration was evident but not significant (22%), and in 1 patient the AVM was unchanged. Other angiographic features in incompletely obliterated cases were a significant reduction of flow velocity through the malformation together with a reduction in diameter of both feeding arteries and draining veins.

Adolescent↗
PubMed1989

[Malignant hyperthermia. A case with minimal manifestations].

A case of malignant hyperthermia is reported. The clinical symptoms arised after anesthesia and the post-operative enzymatic alterations prompted the Authors to send the patient to the University of Padua where muscle byopsy and caffeine contracture test were performed. The initial diagnosis was confirmed.

Adult↗
PubMed1988

Age and sex related changes of plasma membrane fluidity in isolated rat hepatocytes.

The influence of sex and age on membrane fluidity, has been investigated in 6, 12, 18 weeks old Sprague-Dawley rats. Fluorescence polarization (P) was determined at 37 degrees C with a Perkin Elmer MPF 44A fluorescence spectrophotometer. The fluorescent probe TMA-DPH was added to isolated hepatocytes prepared by collagenase method. The membrane fluidity was constantly lower in males than in females, but the difference was statistically significant only in the 12 weeks old group. Major differences appeared related to aging with a significant age-related decrease in fluidity in all animals.

Aging↗
PubMed1988

4-Hydroxynonenal and other lipid peroxidation products are formed in mouse liver following intoxication with allyl alcohol.

Some recent reports indicate that lipid peroxidation might play a crucial role in the production of allyl alcohol hepatotoxicity. Previous work from our laboratory has suggested that in the case of bromobenzene, a hepatotoxin sharing the ability of allyl alcohol to induce a marked depletion of liver glutathione, liver injury is likely to be mediated by lipid peroxidation. In particular, we demonstrated that 4-hydroxynonenal and other aldehydes derived from lipid peroxidation can be detected in the liver of bromobenzene-poisoned mice. In the present study, we report also the in vivo formation of 4-hydroxynonenal and other aldehydes after allyl alcohol poisoning. 24-h-fasted mice were intoxicated with allyl alcohol (1.5 mmol/kg body wt., i.p.) and killed 1-3 h later. 4-Hydroxynonenal and other carbonyls were looked for in liver extracts in the form of 2,4-dinitrophenylhydrazone derivatives. After fractionation of liver extracts by means of thin-layer chromatography (TLC), a well-resolved peak corresponding to standard 4-hydroxynonenal was obtained in the high-pressure liquid chromatography analysis. Total carbonyls (as 2,4-dinitrophenylhydrazones) were separated by TLC into three fractions, according to their different polarity. The amounts of carbonyls present in each fraction were determined by ultraviolet-visible spectroscopy. In addition, several products were identified in the fraction of the 'non-polar carbonyls' corresponding to alkanals and alk-2-enals.

1-Propanol↗
PubMed1988

MgATP-dependent glucose 6-phosphate-stimulated Ca2+ accumulation in liver microsomal fractions. Effects of inositol 1,4,5-trisphosphate and GTP.

Ca2+ release triggered by inositol 1,4,5-trisphosphate (IP3) and/or GTP has been studied with rough and smooth microsomes isolated from rat liver. Microsomes were loaded with Ca2+ in the presence of MgATP and in the presence or in the absence of glucose 6-phosphate (glucose-6-P) which markedly stimulated the MgATP-dependent Ca2+ accumulation in rough and smooth microsomes (5- and 10-fold, respectively). Upon addition of IP3 (5 microM), rough and smooth microsomes rapidly release a part (not exceeding 20%) of the Ca2+ previously accumulated both in the absence and in the presence of glucose-6-P. Under the same experimental conditions, inositol 1,3,4,5-tetrakisphosphate was ineffective in triggering any Ca2+ release. Upon addition of GTP (10 microM) both the microsomal fractions progressively release the Ca2+ previously accumulated in the presence of glucose-6-P, when 3% polyethylene glycol was also present. In the absence of polyethylene glycol, GTP released Ca2+ from rough microsomes only, and GTP plus IP3 caused a Ca2+ release which was the sum of the Ca2+ releases caused by GTP and IP3 independently. Both IP3 and GTP, added to microsomes at the beginning of the glucose-6-P-stimulated Ca2+ uptake, reduced the Ca2+ accumulation into rough and smooth microsomes without modifying the initial rate (3 min) of Ca2+ uptake. Also in these conditions, the effects of GTP and IP3 were merely additive. These results indicate that both rough and smooth liver microsomes are responsive to IP3 and GTP with respect to Ca2+ release and that IP3 and GTP likely act independently.

Adenosine Triphosphate↗
PubMed1988

Validity of stereotactic biopsy as a diagnostic tool.

254 patients affected by intracranial lesions underwent stereotactic biopsy in our department from 1978 to 1986. Target localization was achieved by CT. Multiple biopsy sampling was performed by cup microforceps or sliding cannula. Operative mortality was limited to 2 cases. Definitive tumour diagnosis including type and approximate grading was obtained in 211 (83%) patients. Diagnostic failures have been investigated from the neuroradiological point of view. Failure rate is low in solid tumours with CT homogeneous appearance and clear-cut borders, gradually increases in non homogeneous tumours, necrotic haemorrhagic or cystic, and is high in non classifiable lesions, generally hypodense at CT, with indefinite borders. In the authors opinion the variability of diagnostic retrieval in different types of lesions must be taken into account when proposing stereotactic biopsy.

Biopsy↗
PubMed1988

Computed tomography after lumbar disc surgery: a comparison between symptomatic and asymptomatic patients.

The evaluation of patients with recurrent symptoms after lumbar disc surgery, is a difficult diagnostic problem. The causes of failure may include recurrent disc herniation, postoperative scarring, arachnoiditis, spinal stenosis, infection and mechanical instability. The most common causes are recurrent herniation and postoperative scarring; the routine x-ray and myelographic differentiation between them is difficult or impossible. High resolution CT has shown some results in the evaluation of the postoperative patients. It requires some knowledge of CT findings of "normal" pictures of the physiologic healing and scarring after disc surgery. We scanned 30 asymptomatic operated patients and 30 patients with recurrent sciatic nerve pain after disc surgery. From our observations result that it is quite impossible to distinguish "normal" scar from asymptomatic fibrosis. The degree and type of fibrosis are not related to recurrent symptoms.

Adult↗
PubMed1988

Primary familial hypoparathyroidism with an autosomal dominant mode of inheritance.

A family with primary isolated hypoparathyroidism transmitted by an autosomal dominant gene was documented; the proband was a 38-year-old woman with a history of weakness and carpopedal spasm. The family study revealed that 6 out of 13 members belonging to 3 generations were affected by hypoparathyroidism without any evidence of an autoimmune disease. Vertical male-to-male, female-to-female and female-to-male transmission were demonstrated. Having excluded the recessive form of familial hypoparathyroidism, pseudohypoparathyroidism, primary familial hypomagnesemia and any immunological disorder, the autosomal dominant inheritance seems to be the most important etiology of idiopathic hypoparathyroidism.

Adolescent↗