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Biomedical subjects

M Iannone

Publications and source records attributed to M Iannone.

27 records · Page 2Linked to original sources
PubMed1991

Ultrafast infrared spectroscopy of bacteriorhodopsin.

Picosecond infrared spectroscopy is developed and used for the first time to study the dynamics of photoexcited bacteriorhodopsin (BR). Both spectral and time-resolved data are obtained. The results open an entirely new approach to investigations of the BR photocycle. The infrared difference spectrum (K minus BR570) recorded at ambient temperature between 1,560 and 1,700 cm-1 is not identical with the spectrum reported for a frozen sample. Three bands of the K state at 1,622, 1,610, and 1,580 cm-1 and the bleaching at 1,637 cm-1 (C = NH stretch) are seen. These new spectral lines appear in less than 10 ps.

Bacteriorhodopsins↗
PubMed1991

Bilateral carotid occlusion in normotensive rats: olds facts and new observations.

This work describes that prolonged mild cerebral ischemia may lead to either general or regional derangement of brain morphofunctional integrity. Normotensive adult Wistar rats were used. Under anesthesia with volatile agents or thiopental, the common carotid arteries were ligated permanently. In one group of animals local cerebral blood flow (1CBF) was measured two hours after carotid occlusion using the [14C]iodoantipyrine method. The other carotid-occluded animals were used for clinical rating and histological evaluation, which was performed two days to 4 weeks after surgical operation. The [14C]iodoantipyrine method showed widespread reduction in the cerebral circulation of carotid-occluded animals. Several hours after carotid occlusion, 40% of the animals showed dramatic neurological signs and died on the day of operation. In 35% of surviving animals, brain infarctions were observed in one and exceptionally two areas of the sensorimotor cortex, thalamus, hippocampus or cerebellum. The evolutionary sequence of the histopathological changes seems to date the induction of the infarcts to the early period of carotid occlusion. In conclusion, reduction of cerebral blood flow causes, in a high percentage of animals, various degrees of acute brain damage after an apparent symptom-free interval.

Animals↗
PubMed1990

Increased serum selenium levels in patients under corticosteroid treatment.

The normal serum and tissue levels of many micronutrients are remarkably affected by the therapeutical administration of several substances. In the present study, we have evaluated the modifications of serum selenium levels in different groups of patients under corticosteroid treatment. Such therapy was significantly associated with increased serum selenium levels, with a dose-dependent relationship in subjects treated with methylprednisolone. The reasons for this association are unknown. However, a reduced renal excretion of selenium, due to the mineralcorticoid activity of the corticosteroids, can be inferred.

Adult↗
PubMed1986

Sperm maturation in human semen: role of transglutaminase-mediated reactions.

A Ca2+-dependent, transglutaminase-like activity has been detected both free in the human seminal plasma and bound on the spermatozoon surface. A marked variability of the two enzymatic activities in the semen of different normal subjects was observed; but limited changes occurred in various ejaculates of the same individual. Moreover, we report evidence of the ability of several seminal plasma proteins to act as acyl donor substrates for endogenous transglutaminase, whereas human ejaculated spermatozoa have been shown to possess polyamine-binding sites specifically involved in transglutaminase-catalyzed reactions. It is postulated that semen transglutaminase may play a role in suppressing sperm antigenicity and in the male gamete's acquiring biological features of a fully differentiated and fertile cell.

Adult↗
PubMed1984

3-Deazaadenosine. S-adenosylhomocysteine hydrolase-independent mechanism of action in mouse lymphocytes.

3-Deazaadenosine (c3Ado) inhibits the ability of specifically sensitized mouse lymphocytes to lyse tumor cells, and this effect of c3Ado on immune function is accompanied by a buildup of both S-adenosylhomocysteine (AdoHcy) and S-3-deazaadenosylhomocysteine (c3AdoHcy) within the lymphocytes (Zimmerman, T. P., Wolberg, G., and Duncan, G. S. (1978) Proc. Natl. Acad. Sci. U.S.A. 75, 6220-6224). Several types of evidence have now been obtained which indicate that neither of these latter two biochemical events contributes to this biological activity of c3Ado. First, periodate-oxidized adenosine (Adox) and 3-deaza(+/-)aristeromycin, two compounds which are not inhibitory to this lymphocyte function, were both more effective than c3Ado in elevating lymphocyte AdoHcy levels and in inhibiting protein carboxymethylation within these cells. Second, pretreatment of lymphocytes with Adox (to inhibit AdoHcy hydrolase) prevented the metabolic formation of c3AdoHcy during subsequent incubation of the cells with c3Ado without diminishment of the biological activity of c3Ado. Third, the lymphocyte buildup of c3AdoHcy exhibited a concentration dependence upon c3Ado which was biphasic and greatly dissimilar to that for the inhibition of lymphocyte function by c3Ado. These results are not compatible with the widely held view that c3Ado, as a single agent, affects various cellular functions as a consequence of elevations in intracellular AdoHcy and/or c3AdoHcy and suggest that c3Ado inhibits this particular lymphocyte function by an unknown mechanism which is independent of the interaction of c3Ado with AdoHcy hydrolase. During this study, it was found that pretreatment of lymphocytes with Adox prevented the potentiation by homocysteine of this immunoinhibitory activity of c3Ado and reduced the biological effect of the c3Ado/homocysteine combination to that observed with c3Ado alone. This result indicates that the ability of homocysteine to potentiate this biological activity of c3Ado requires the metabolic formation of c3AdoHcy catalyzed by AdoHcy hydrolase.

Adenosylhomocysteinase↗
PubMedDate not supplied

N omega-nitro-L-arginine-methyl ester inhibits electrocortical recovery subsequent to transient global brain ischemia in Mongolian gerbil.

Electrocorticographic (ECoG) activity remains isoelectric for about 15 min after transient (10 min) bilateral carotid arteries occlusion in mongolian gerbils. In this model of global forebrain ischemia N omega-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly delays the recovery of ECoG amplitude. Thus, the present experiments suggest that NO is involved in the cerebrovascular physiological response to brain ischemia.

Animals↗