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Biomedical subjects

A Benedetti

Publications and source records attributed to A Benedetti.

At least 217 records · Page 12Linked to original sources
PubMed1981

A new method for utilizing CT data in stereotactic surgery: measurement and transformation technique.

The proposed system is essentially based on the definition of a coordinate system, rigidly connected with the skull, by the introduction of three reference X-ray opaque points, secured into the bone of the skull. Target and reference points CT coordinates are given by the image display console. The three reference points are also identified on stereoradiographs, and their actual stereotactic coordinates are calculated by a geometrical approach which takes into account radiological distortion. A programmed computer links the target, identified on tomograms, to the three points system and calculates its stereotactic coordinates.

Humans↗
PubMed1981

Inhibition of protein synthesis by carbonyl compounds (4-hydroxyalkenals) originating from the peroxidation of liver microsomal lipids.

Carbonyl compounds released during the NADPH-Fe dependent peroxidation of liver microsomal lipids and identified as 4-hydroxyalkenals (almost entirely as 4-hydroxynonenal) inhibit protein synthesis in a rabbit reticulocyte lysate. The ID50 was 0.48 mM. The inhibitory effect was reproduced by synthetic 4-hydroxynonenal. The inhibition was already evident at 1-2 min of incubation. The addition of -SH groups to the incubation medium afforded a marked protection against the inhibition of protein synthesis. The inhibitory effect seems to be due to an interaction of the carbonyl compound with -SH groups essential for the cellular protein synthetic machinery.

Aldehydes↗
PubMed1981

Spinal surgery for spasticity (46 cases).

The authors report their experiences in the surgical treatment of spastic syndromes by operations on the spinal cord and nerve roots. In the authors' neurosurgical department 20 lumbar myelotomies, 19 posterior selective lumbar rhizotomies, 2 complete posterior lumbar rhizotomies, 4 anterior lumbar rhizotomies and five posterior cervical rhizotomies were performed. Clinical results can be considered good on the whole. There was no mortality and no major complication in the entire series. The effect of selective posterior lumbar rhizotomy on the evolution of cerebropathic spastic paraparesis was particularly impressive. Six of 46 patients experienced a late recurrence of spasticity, but they all had good results after a further operation. The particular criteria for selection of each surgical procedure are discussed and related to the aetiology and clinical picture of the spastic syndrome.

Adolescent↗
PubMed1980

Identification of 4-hydroxynonenal as a cytotoxic product originating from the peroxidation of liver microsomal lipids.

During the NADPH-Fe induced peroxidation of liver microsomal lipids, products are formed which show various cytopathological effects including inhibition of microsomal glucose-6-phosphatase. The major cytotoxic substance has been isolated and identified as 4-hydroxy-2,3-trans-nonenal. The structure was ascertained by means of ultraviolet, infrared and mass spectrometry and high-pressure liquid chromatographic analysis. Moreover, 4-hydroxynonenal, prepared by chemical synthesis, was found to reproduce the biological effects brought about by the biogenic aldehyde. Preliminary investigations suggest that as compared to 4-hydroxynonenal very low amounts of other 4-hydroxyalkenals, namely 4-hydroxyoctenal, 4-hydroxydecenal and 4-hydroxyundecenal are also formed by actively peroxidizing liver microsomes. In the absence of NADPH-Fe liver microsomes produced only minute amounts of 4-hydroxyalkenals. The biochemical and biological effects of synthetic 4-hydroxyalkenals have been studied in great detail in the past. The results of these investigations together with the finding that 4-hydroxyalkenals, in particular 4-hydroxynonenal, are formed during NADPH-Fe stimulated peroxidation of liver microsomal lipids, may help to elucidate the mechanism by which lipid peroxidation causes deleterious effects on cells and cell constituents.

Aldehydes↗
PubMed1980

The broken clip.

A case of a broken clip demonstrated by radiography is presented. As angiography showed no filling of the aneurysm, further operation was not considered necessary. The cause of the fracturing of the clip remains unknown.

Female↗
PubMed1980

Effects of carbonyl compounds (4-hydroxyalkenals) originating from the peroxidation of liver microsomal lipids on various microsomal enzyme activities of the liver.

Carbonyl compounds released during the NADPH-Fe dependent peroxidation of liver microsomal lipids and identified as 4-hydroxyalkenals (almost entirely as 4-hydroxynonenal) while inhibiting microsomal enzymes (such as glucose 6-phosphatase and aminopyrine demethylase) which are affected by lipid peroxidation, have no effect on microsomal NADPH-cytochrome c reductase. The latter enzyme activity is unaffected (or even increased) when liver microsomes are allowed to peroxidize in the NADPH-Fe dependent system. NADPH-cytochrome c reductase, contrary to the other enzymes, is similarly unaffected after CCl4 poisoning, that is in a situation in which peroxidation of membrane lipids of liver endoplasmic reticulum has been unequivocally demonstrated. It appears therefore that the effects exherted by lipid peroxidation or by 4-hydroxyalkenals originating from lipid peroxidation parallel the effects of CCl4 intoxication in vivo.

Aldehydes↗
PubMed1979

Effects of diffusible products of peroxidation of rat liver microsomal lipids.

The effects on cellular structures of products of peroxidation of rat liver microsomal lipids were investigated. A system containing actively peroxidizing liver microsomal fraction was separated from a revealing or target system by a dialysis membrane. The target system, contained in the dialysis tube, consisted of either intact cells (erythrocytes) or subcellular fractions (liver microsomal fraction). When liver microsomal fractions were incubated with NADPH (or an NADPH-generating system), lipid peroxidation, as measured by the amount of malonaldehyde formed, occurred very rapidly. The malon-aldehyde concentration tended to equilibrate across the dialysis membrane. When the target system consisted of erythrocytes, haemolysis occurred abruptly after a lag phase. The lysis was greatly accelerated when erythrocytes from vitamin E-deficient rats were used, but no haemolysis was observed when erythrocytes from vitamin E-treated rats were used. When, in the same system, freshly prepared liver microsomal fractions were exposed to diffusible factors produced by lipid peroxidation, the glucose 6-phosphatase activity markedly decreased. A similar decrease in glucose 6-phosphatase activity, as well as a smaller but significant decrease in cytochrome P-450, was observed when the target microsomal fractions were exposed to diffusible factors derived from the peroxidation of liver microsomal lipids in a separate preincubation step. These and additional experiments indicated that the toxicological activity is relatively stable. Experiments in which the hepatic microsomal fractions destined for lipid peroxidation contained radioactively labelled arachidonic acid, previously incorporated into the membranes, showed that part of the radioactivity released from the microsomal fraction into the incubation medium entered the dialysis tube and was recovered bound to the constituents of the microsomal fractions of the target system. These results indicate that during the course of the peroxidation of liver microsomal lipids toxic products are formed that are able to induce pathological effects at distant loci.

Animals↗
PubMed1979

Binding of products originating from the peroxidation of liver microsomal lipids to the non-lipid constituents of the microsomal membrane.

The binding of products derived from the peroxidation of liver microsomal lipids to the non-lipid constituents of the microsomes was studied. To this end arachidonic acid labelled with tritium at the positions of the double bonds was given to rats and allowed to incorporate into the membrane lipids of the liver cell. When liver microsomes containing labelled arachidonic acid were incubated aerobically in the NADPH-dependent system, a marked production of malonic dialdehyde (MDA) occurred and, concomitantly, there was a consistent release of radioactivity from the microsomes into the incubation medium. The addition of EDTA to the incubation medium prevented, to a large extent, both the MDA formation and the release of radioactivity. Chromatographic studies showed that the bulk of the radioactivity released from the incubated microsomes is not MDA. In the incubated microsomes, the radioactivity decreased in total lipids, while it increased by about 15 times in the non-lipoidal residue. A similar increase in radioactivity was seen in microsomal protein, while no increase was observed in microsomal RNA (the radioactivity was negligible in both the incubated and the non-incubated samples). It seems therefore that products originating from lipoperoxidation of arachidonic acid covalently bind to the microsomal protein. In order to investigate whether alterations similar to those observed in the in vitro peroxidation of liver microsomes could be detected in the in vivo intoxication with carbon tetrachloride, rats given labelled arachidonic acid as above, were poisoned with CCl4. Sixty minutes after poisoning, the radioactivity present in the microsomal lipids was generally lower in the intoxicated rats than in the controls, while the labelling of the non-lipoidal residue and of the protein was higher in the CCl4-poisoned rats.

Animals↗
PubMed1978

Free radical damage produced by carbon tetrachloride in the lipids of various rat tissues.

Alterations produced by carbon tetrachloride in the lipids of extrahepatic tissues were studied. Consistent incorporation (about one-half of that occurring in the liver) of 14C from 14CCl4 was found in the phospholipids of the intestinal mucosa; kidney, adrenal and lung phospholipids were labeled to a lower extent, while spleen, testis, brain, heart and skeletal muscle lipids showed minor levels of radioactivity. The analysis of fatty acid methyl esters derived from phospholipids by gas-liquid chromatography (GLC) with an electron capture detector (ECD), showed ECD response similar to that observed with the liver, in the case of the intestinal mucosa and the kidney; on the contary no ECD response was seen with the organs, such as skeletal muscle, heart and testis in which the incorporation is almost negligible. Unlike liver phospholipids, the phospholipids of the intestinal mucosa and the kidney did not show diene conjugation absorption. Also, no evidence of lipid peroxidation was found in the thin-layer chromatographic analysis of fatty acid methyl esters prepared from the phospholipids of these organs. Possible meanings of these results are discussed.

Animals↗