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Biomedical subjects

L Guarini

Publications and source records attributed to L Guarini.

At least 37 records · Page 2Linked to original sources

Transsulfuration by human long term lymphoid lines. Normal and cystathionase-deficient cells.

Long term human lymphoid cells from normal subjects were able to convert [35S]homocysteine to [35S]-cystine. The labeled cystine was found incorporated into proteins. Cells cultured from a patient with vitamin B6-unresponsive cystathioninuria, which contain no measurable cystathionase activity, were unable to perform this conversion. This is the first direct demonstration of transsulfuration by diploid cells in culture.

Cell Line↗

Histidyl-tRNA synthetase from Salmonella typhimurium: specificity in the binding of histidine analogues.

The topography of the active site of histidyl-tRNA synthetase has been investigated by determining Ki values for a variety of structural analogues of histidine, using the ATP-PPi exchange and tRNA aminoacylation reactions. Using these kinetic constants it has been possible to have a measure of the relative binding affinity of the enzyme for the histidine analogues. The following conclusions have been drawn: (a) the enzyme is stereospecific in the formation of aminoacyl-tRNA complexes, since the D-isomer of histidine does not influence the two reactions; (b) the carboxyl group is not required for binding; (c) bulky derivatives of the carboxyl group prevent the molecules from binding to the enzyme; (d) the amino group permits a good binding affinity; (e) the length of the ring side chain plays a very important role as point of attachment to the enzyme; (f) the kinds of heteroatoms on the ring determine the inhibitory properties of the analogues.

Adenosine Triphosphate↗

Standing to lying heart rate variation. A new simple test in the diagnosis of diabetic autonomic neuropathy.

We have examined the immediate heart-rate response to standing to lying (S-L) in 83 male insulin-dependent diabetic subjects aged 40 +/- 11 years (mean +/-S.D.) who underwent five other cardiovascular autonomic tests. Using a specially devised scoring system, the patients were divided into 3 groups: 54 subjects without autonomic neuropathy; 17 'borderlines'; 12 with autonomic neuropathy. The results were compared with those of 50 sex and age matched controls. We evaluated: S-L1 = ratio between R-R mean before lying and R-R minimum over the first 5 beats after lying; S-L2 = ratio between R-R maximum between the 20th to 25th beat and R-R minimum over the first 5 beats after lying. In controls S-L1 was 1.23 +/- 0.098 (mean +/- S.D.), S-L2 1.56 +/- 0.2. In diabetic subjects without autonomic neuropathy S-L1 was 1.18 +/- 0.096 (p less than 0.01), S-L2 1.50 +/- 0.23. In the autonomic group S-L1 was 1.03 +/- 0.01 (p less than 0.001), S-L2 1.16 +/- 0.086 (p less than 0.001). We propose that the lowest normal and highest abnormal limits of S-L1 are 1.10 and 1.07, respectively, and that normal and highest abnormal limits of S-L2 are 1.23 and 1.41, respectively. We suggest the use of S-L1 as a pure parasympathetic test and S-L2 as a mixed but predominantly sympathetic test in the diagnosis of autonomic neuropathy.

Adult↗

Evaluation of the vagal-sympathetic interaction in diabetics with autonomic neuropathy through power spectrum density analysis of the heart rate. A critical revision of the natural history of diabetic autonomic neuropathy is possible.

In this paper we apply spectral analysis methods to heart rate variability to assess the autonomic nervous system activity in normal subjects and in patients affected by different degrees of diabetic autonomic neuropathy. The current opinion, based on different clinical tests, is that parasympathetic impairment occurs earlier in autonomic dysfunctions. However, the use of power spectrum density analysis based on a single parameter (heart rate) suggests a simultaneous involvement of parasympathetic and sympathetic pathways leading to the conclusion that perhaps the natural history of diabetic autonomic neuropathy should be substantially rewritten.

Autonomic Nervous System Diseases↗