ACTA ENDOCRINOLOGICA (BUC)

OBJECTIVES: This study was carried out on 1290 patients, whose choroids plexus and pineal gland were examined on computed tomography. Aim: To check the correspondence between the choroid plexuses and the pineal gland calcifications along age groups and sex; and the connections between these calcifications and associated pathology.\r\nMATERIALS AND METHODS: The study group consisted of patients of both sexes, within six age intervals.\r\nRESULTS: In order to classify the calcification variants, eight types of combinations were ordered and can be seen in CT: two refer to extreme variants: totally uncalcified (type 1) and totally calcified (type 8); bilateral, symmetrical variants (types 4 and 5); the other four types include the asymmetrical calcifications (2, 3, 6 and 7). After the anthropological study the results demonstrate that there are significant differences between calcification of the choroids plexus and those of the pineal gland with the two sexes, on age groups and pathological ground. For type 1-totally uncalcified the maximum frequency is around 70% with ages under 19. For type 8 - totally calcified, bilateral, the maximum frequency is around 50% with age groups 48-59 and 60-71. For type 4 - calcification only of choroid plexus, one finds a continuous increase from about 10% at the first age group to about 25% at the last group, while for type 5- calcification only of the pineal gland the frequency is 10%−20%. We started from the hypothesis that the presence of these calcifications is physiological, and has an active adaptative metabolic part depending on many factors, among which the individual constitutional ground is also present.\r\nCONCLUSIONS: The age is not the main cause of the calcification types, but a process of adaptative-reactive variability of interface type, playing an integrating mediating part.

Background. The pro-thrombotic potential of the anabolic androgenic steroids (AAS), worldwide misused substances, has increasingly become a subject of current interest. Conversely, taurine, a sulfur-amino acid ubiquitous in human body, in addition to other beneficial effects, is thought to have an inhibitory effect on platelet aggregation. Purpose. To assess platelet aggregation both taurine and high doses of AAS were simultaneously chronically administered in rats. Methods. The experiment was conducted on 40 male Wistar rats, divided into 4 equal groups: control (C) – no treatment; AAS (A) – treated with 10 mg/kg/week of nandrolone decanoate (DECA); taurine (T) – daily treated with oral supplementation of 2% taurine in drinking water; androgen and taurine group (AT) – concomitant administration of DECA and taurine. After 12 weeks of treatment, blood samples were collected and platelet aggregation induced by ADP was performed using the turbidimetric method. Results. The platelet aggregation magnitude was significantly higher (p<0.001) in group A (62.1±6.10%) than in group C (47.8±5.39%), while in group T (40.3±6.49%) it was significantly lower (p=0.04). Moreover, the platelet aggregation response was significantly lower in group AT (54.5±6.38%) than in group A (p=0.04), without a significant difference between group AT and group C (p=0.08). Conclusion. Our findings provide additional evidence regarding harmful potential of high doses of DECA, chronically administered. The increased platelet aggregation induced by AAS may be decreased by diet supplementation with taurine.

Context. Foetal asphyxia, a frequent birth complication, detrimentally impacts the immature brain, resulting in neuronal damage, uncontrolled seizure activity and long-term neurological deficits. Oxytocin, a neurohormone mediating important materno-foetal interactions and parturition, has been previously suggested to modulate the immature brain’s excitability, playing a neuroprotective role. Our aim was to investigate the effects of exogenous oxytocin administration on seizure burden and acute brain injury in a perinatal model of asphyxia in rats. Animals and methods. Asphyxia was modelled by exposing immature rats to a 90-minute episode of low oxygen (9% O2) and high CO2 (20% CO2). Control rats were kept in ambient room-air for the same time interval. In a third group of experiments, oxytocin (0.02 UI/g body weight) was nasally administered 30 minutes before the asphyxia episode. Seizure burden was assessed by the cumulative number of loss of righting reflex (LRR) over a two-hour postexposure period. Acute brain injury was assessed through hippocampal S-100 beta, a biomarker of cellular injury, 24-hours after exposure. Results. Asphyxia increased both LRR and hippocampal S-100 beta protein compared to controls, and these effects were significantly reduced by oxytocin administration. Conclusion. Oxytocin treatment decreased both seizure burden and hippocampal injury, supporting a potential neuroprotective role for oxytocin in perinatal asphyxia.