Biomedical subjects

Luis Martins

Publications and source records attributed to Luis Martins.

5 recordsLinked to original sources

PubMed2006

Mapping cellular gains and losses in the postnatal dentate gyrus: implications for psychiatric disorders.

Neurogenesis and apoptosis occur contemporaneously in the postnatal hippocampal dentate gyrus and have been implicated in mood and cognitive disorders. Particularly, neurogenesis correlates with the manifestation of antidepressant effects, but its quantitative and topographical relationship with concomitant cell death has not been investigated. Accordingly, we applied stereological measurements to obtain synchronized topographical maps of these two events in rats aged 1 and 3 months under basal conditions; the two ages were chosen to represent neuro-developmental windows during which cell proliferation and death are occurring at peak and relatively steady levels, respectively. Our analysis shows that apoptotic cells are evenly distributed throughout the dentate gyrus, although the incidence of apoptosis decreased gradient-wise from the tip of the suprapyramidal layer and was highest in the external third of the granule cell layer. Interestingly, apoptosis was higher in the left hippocampus. In addition, we confirm previous less stringent studies demonstrating that neurogenesis occurs differentially in the dorsal-ventral axis of the hippocampus and in suprapyramidal-infrapyramidal blades of the dentate gyrus. These results raise intriguing new questions regarding the coordinated regulation of hippocampal neurogenesis and apoptosis since the two processes apparently share common regulatory factors. In addition, these findings open questions with respect to the functional significance of topographical gradients in neurogenesis and apoptosis in the context of the etiopathogenesis of neuropsychiatric diseases and the reported dependence on the efficacy of therapeutic agents on the generation of new hippocampal neurons.

Age Factors↗

PubMed2006

Attenuation of heart rate recovery after exercise in hypertensive patients with blunting of the nighttime blood pressure fall.

OBJECTIVES: To evaluate whether hypertensive patients with attenuation of nighttime blood pressure (BP) fall exhibit a delay of the recovery of heart rate (HR) after exercise as an index of a general decrease in the vagal tone. METHODS: Mild-moderate hypertensive patients (n = 219, age 55 +/- 3, 77% men) underwent a maximal exercise test (Bruce > 85% heart rate limited) in whom we calculated the recovery of HR as the percent decrease of HR from peak to 1 min after stopping exercise (%HR fall-1 min), a 24-h ambulatory BP monitoring, calculating the percent decrease of nighttime vs. daytime BP (% night SBP fall). Left ventricular mass index (LVMI) was measured by echo and aortic stiffness by pulse wave velocity (PWV). Sixty percent were on antihypertensive drugs (not on beta-blockers nor on non-dihydropiridine calcium blockers); 12 subjects were type 2 diabetics. RESULTS: The "% night SBP fall" ranged from - 6.3% to 38.9% and the "%HR fall-1 min" ranged from 3.3% to 43.7%. There was a significant positive correlation between these two variables (r = 0.594, p < 0.001). Population was divided into five groups according to quintiles of values for the "% night SBP fall". For similar daytime BP and age, the lowest quintile for % night SBP fall (- 6.3% to 7.2%) showed the lower "%HR fall-1 min" (3.1 +/- 0.5%), and the higher LVMI (92 +/- 3 g/m(2)) and PWV (12.1 +/- 0.4 m/s) values comparing to the other quintiles (p < 0.02). CONCLUSIONS: In hypertensives, blunting of the nocturnal fall of BP is associated with a delayed recovery in heart rate after graded maximal exercise and with greater aortic stiffness and ventricular mass. This may indicate that in non-dipper subjects a relative general decrease of parasympathetic reactivation after exercise is linked to the failure of nighttime fall of BP, both of which might contribute to target-organs deterioration.

Analysis of Variance↗

PubMed2004

Cellular inactivation and chromosomal aberrations: initial damage.

It has been proposed that unrepaired or misrepaired complex lesions of DNA are responsible for cell inactivation and chromosomal aberrations. The detailed features of the critical damage and the nature of initiating physical events are actively investigated. We studied the role of inner-shell (core) ionizations in DNA atoms is studied. Ultrasoft X-rays from LURE synchrotron radiation have been used to mimic core events induced by ionizing radiations. For biological matter, inner-shell photoionization is indeed the main interaction channel of these radiations. Moreover, by tuning the X-ray energy below and above the carbon K-threshold, it is possible to achieve a two-fold increase in the number of core-ionizations in DNA for a same dose. Cell survival and chromosome aberrations have thus been studied at three iso-attenuated energies: 250, 350, and 810 eV. Relative biological efficiencies (RBEs) for cell inactivation and chromosome aberrations were found to be strongly correlated with the yields of core events in DNA.

Animals↗

PubMed2002

Human telomeric position effect is determined by chromosomal context and telomeric chromatin integrity.

We investigated the influence of telomere proximity and composition on the expression of an EGFP reporter gene in human cells. In transient transfection assays, telomeric DNA does not repress EGFP but rather slightly increases its expression. In contrast, in stable cell lines, the same reporter construct is repressed when inserted at a subtelomeric location. The telomeric repression is transiently alleviated by increasing the dosage of the TTAGGG repeat factor 1 (TRF1). Upon a prolongated treatment with trichostatin A, the derepression of the subtelomeric reporter gene correlates with the delocalization of HP1alpha and HP1beta. In contrast, treating the cells with 5 azacytidin, a demethylating agent, or with sirtinol, an inhibitor of the Sir2 family of deacetylase, has no apparent effect on telomeric repression. Overall, position effects at human chromosome ends are dependent on a specific higher-order organization of the telomeric chromatin. The possible involvement of HP1 isoforms is discussed.

Chromatin↗

PubMedDate not supplied

[Morbidity following cardiac surgery. A proposal for qualification].

The authors propose a new scoring table to quantify morbidity events related to cardiac surgery. They intend to quantify the relative impact of each occurred event and also to calculate and score the sum of all morbidity events occurring in a given patient. The table was constructed based on the opinion of a panel of international experts that were asked to quantify the morbidity events on the proposed list. Their answers were integrated and analyzed according to the inferring Delphi's method, in order to establish the relative weight of each event, scoring events for each system. The methodology that was adopted is throughly discussed and speculation is made over the use of the table score for related morbidity in cardiac surgery, namely as a tool to compare both the surgical performance and for quality ranking. The scoring table is now being tested clinically.

Cardiac Surgical Procedures↗