Dietary supplements and medications in elite sport--polypharmacy or real need?

The aim of this study was to describe qualitatively and quantitatively dietary supplements (DS) and medication use in elite athletes. Athletes (n=912; age 23.9 ± 6 years; 72% male) reported medications and DSs taken within 3 days before doping control. We analyzed data collected from 2006 to 2008, identified and classified substances. Total of 74.6% athletes reported use of at least one substance, 61.2% took DS (3.17 per user) and 40.6% took medications. Among users, 21.2% reported the use of six and more different products, and one took 17 different products at the same time. Majority of medication users took non-steroidal anti-inflammatory drugs (NSAID) (24.7%), and 22.2% used more than one NSAID. We found no gender differences in DS use (P=0.83). Individual sport athletes used more DS (P<0.01). Our study showed widespread use of DS and drugs by elite athletes. Consumption of DS with no evident performance or health benefits, demonstrated the need for specific educational programs focused on DS use. Amount, quantity and combination of the reported products raised concern about the risk of potential side effects.

Effects of NMDA receptor blockade in the developing rat somatosensory cortex on the expression of the glia-derived extracellular matrix glycoprotein tenascin-C.

The patterning of synaptic connections during development is thought to be influenced by the correlation of neuronal impulse activity. N-methyl-D-aspartate (NMDA) receptors have been implicated in the reorganization of thalamocortical afferents in the visual system. The topographic mapping of the periphery of sensory systems onto the somatosensory cortex in the whisker-barrel field of rodents has served as another important paradigm in the study of extrinsic influences on synaptic rearrangements. In a search for the molecular cues that may contribute to synaptic plasticity, we have investigated the distribution of the glia-derived extracellular matrix glycoprotein tenascin-C, which is highly expressed during the formation of the barrel field map around birth and delineates the boundaries between barrel fields after segregation of afferent inputs. Here we show that systemic and local application of NMDA receptor antagonists at postnatal day 2 inhibited the down-regulation of tenascin mRNA and protein by postnatal day 6 and prevented the appearance of tenascin-positive barrel field boundaries. Furthermore, barrels were not distinguishable by Nissl staining, and segregation of thalamocortical afferents as monitored by anterograde Dil tracing and acetylcholinesterase histochemistry was not complete. These observations indicate that expression of tenascin-C and segregation of afferent inputs are modified by NMDA receptor-dependent neuronal activity.

Transient expression of NADPH diaphorase activity in the mouse whisker to barrel field pathway.

Development of the topographic map of the somatosensory cortex of rodents appears to depend on fine-tuned patterns of neuronal activity. Nitric oxide (NO) has been described as a potent messenger in the modulation of neural activity associated with synaptic plasticity. To evaluate the role of NO in the murine somatosensory pathway, we investigated NO synthase activity by NADPH diaphorase histochemistry at crucial developmental stages. At birth, NADPH diaphorase activity was detected in the cortical plate of the developing somatosensory cortex. At day 3, diffuse NADPH diaphorase activity increased within the emerging layer 4 in the future barrel field hollows. This staining was most intense at day 6 in the barrel field hollows and became undetectable by the end of the second postnatal week. The appearance of the diffuse NADPH diaphorase staining pattern was also observed in a similar time course and topography in the ascending relays of the somatosensory cortex, specifically in the barreloids within the ventrobasal nucleus of the thalamus and the barrelettes of the trigeminal nucleus of the brainstem. Lesioning the C row of whiskers at day 1 (i.e. during the critical period of barrel formation) led to fused C barrels of diffuse NADPH diaphorase activity in the barrel fields. In addition, highly NADPH diaphorase activity-positive individual cells present in the deeper layers of the somatosensory cortex at days 0 and 3 became visible in the upper layers at day 6 and remained until day 15. In layer 4, these cells were predominantly localized in the septa at day 6 and 9. No positive individual cells were detected in barrelettes or barreloids at any age. We conclude that NADPH diaphorase activity is present during experience-dependent consolidation of synaptic contacts in the somatosensory pathway.

An aspartic acid residue important for voltage-dependent gating of human muscle chloride channels.

A point mutation (D136G) predicting the substitution of glycine for aspartate in position 136 of the human muscle Cl- channel (hClC-1) causes recessive generalized myotonia. Heterologous expression of a recombinant D136G produces functional Cl- channels with profound alterations in voltage-dependent gating, without concomitant changes in pore properties. The mutant exhibits slowly activating current upon hyperpolarization, in contrast to wild-type channels, which display time-dependent current decay (deactivation) at negative membrane potentials. Steady-state activation of D136G depends upon the transmembrane Cl- gradient, reaching zero at voltages positive to the Cl- reversal potential in physiological Cl- distribution. This explains the reduced sarcolemmal Cl- conductance that causes myotonia. The functional disturbances exhibited by D136G may stem from a defect in the ClC-1 voltage sensor.

[Allergic reaction of the lower airways of non asthmatic patients caused by grass pollen]. / Alergijske reakcije donjih disajnih puteva izazvane polenima trava kod neasmaticara.

Having in mind importance of early detection of the disease, in it phase of development, we have reported a case with seasonal allergic rhinitis and allergic reaction of the lower airways in absence of allergic inflammation and clinically evident bronchial asthma.

Seizures can be triggered by stimulating non-cortical structures in the quaking mutant mouse.

Mutant Quaking mice (C57BL/6J) display convulsive tonic-clonic seizures that can be either spontaneous or triggered by manipulation of the animal or by auditory stimulation. Several abnormalities have been found (especially in the noradrenergic system) in the brainstem of this mutant strain. We first verified by electrophysiological recording that the cerebral cortex was not involved in the generation or in the development of these fits. Then we showed that tonic-clonic seizures similar to those obtained in the freely moving animal were triggered by low-threshold (LT, 5-50 microA) or high-threshold (HT, 55-150 microA) stimuli performed during head restraint. LT stimuli were mostly efficient in a number of ponto-bulbar and mesencephalic structures, including several reticular nuclei, the locus coeruleus, the nucleus subcoeruleus and the red nucleus, whereas HT stimuli were generally necessary to trigger fits by stimulating the nuclei pontis, the substantia nigra, the central gray area and the cerebellar nuclei. Seizures were also provoked at the diencephalic level with LT stimulation delivered in the medial thalamic area, the nucleus reticularis thalami and some subthalamic regions (zona incerta, H field of Forel). In contrast, no fits were obtained by stimulating the cerebellar cortex and the inferior colliculus, the ventral and lateral groups of thalamic nuclei or the telencephalic regions (hippocampus, amygdala, caudate nucleus, putamen and cerebral cortex), with the exception of the globus pallidus.