Sleep apnea and comorbid diseases - a review

Obstructive sleep apnea (OSA) is a common disease spreading around the world. It is unavoidably linked to the increasing rate of obesity, particularly in Western societies. Associated higher prevalence of sleep disordered breathing has also been observed. There are many diseases that can lead to OSA and many that are a result of untreated OSA. From the widely known cardiovascular complications to indirectly related diseases, such as insomnia, Alzeihmer’s disease or psoriasis. Overall, sleep-disordered breathing have been shown to negatively impact quality of life, including general health perception, physical functioning, social functioning, and vitality. That is why it is important to spread awareness about OSA, often asymptomatic, through medical staff and patients in the risk group. In this review we describe the illness, the ways to diagnose it and discuss comorbid diseases

Neuroplasticity after injury in the areas of the brain, which are involved in motor control.

The purpose of the thesis was presentation of after injury plastic neural capabilities of the areas of the brain, which are involved in motor control.Brain compensates injuries by changes in structures or by modifications at the cellular level. In damaged motor cortex there is a decreased interhemispheric inhibitory connection which, in the effect, improves cooperation of all structures in both hemispheres.The other alterations happen in the adult cerebellar cortex, inferior olivary neurones show features of structural plasticity in the contrary to the Purkinje cells which display functional plasticity.Every kind of neural plasticity demonstrates natural striving of nervous system to repair. This can be enhanced by appropriate rehabilitative activityCelem pracy było przedstawienie możliwości plastycznych mózgu po przebytym urazie struktur mózgowia zaangażowanych w kontrolę ruchową.Mózg może rekompensować uszkodzenia poprzez działania całych struktur lub modyfikacje na poziomie komórkowym. W uszkodzonej korze ruchowej obserwuje się zmniejszenie mechanizmu hamowania międzypółkulowego, co sprzyja zwiększonej współpracy struktur całości w wykonywaniu danej czynności. Zmiany o innym charakterze zachodzą w obrębie komórek kory móżdżku, gdzie neurony drogi oliwkowo-móżdżkowej wykazują cechy plastyczności strukturalnej w odróżnieniu od komórek Purkinjego, które odznaczają się plastycznością funkcjonalną. Mechanizmy plastyczności struktur mózgowia obrazują naturalne dążenie układu nerwowego do naprawy, które może być wzmacniane przez ukierunkowane działania rehabilitacyjne

Plastoquinone: possible involvement in plant disease resistance.

The plant Solanum nigrum treated with the pathogen Phytophthora infestans-derived elicitor responded by elevated reactive oxygen species (ROS) production, lipid peroxidation and lipoxygenase (EC 1.13.11.12) activity in comparison with control plants indicating that oxidative stress took place. We demonstrate that these events are accompanied by a significant increase in plastoquinone (PQ) level. It is postulated that PQ may be associated with mechanisms maintaining a tightly controlled balance between the accumulation of ROS and antioxidant activity that determines the full expression of effective defence

Alterations of BDNF and trkB mRNA Expression in the 6-Hydroxydopamine-Induced Model of Preclinical Stages of Parkinson’s Disease: An Influence of Chronic Pramipexole in Rats

<div><p>Our recent study has indicated that a moderate lesion of the mesostriatal and mesolimbic pathways in rats, modelling preclinical stages of Parkinson’s disease, induces a depressive-like behaviour which is reversed by chronic treatment with pramipexole. The purpose of the present study was to examine the role of brain derived neurotrophic factor (BDNF) signalling in the aforementioned model of depression. Therefore, we investigated the influence of 6-hydoxydopamine (6-OHDA) administration into the ventral region of the caudate-putamen on mRNA levels of BDNF and tropomyosin-related kinase B (trkB) receptor. The BDNF and trkB mRNA levels were determined in the nigrostriatal and limbic structures by <i>in situ</i> hybridization 2 weeks after the operation. Pramipexole (1 mg/kg sc twice a day) and imipramine (10 mg/kg ip once a day) were injected for 2 weeks. The lesion lowered the BDNF and trkB mRNA levels in the hippocampus [CA1, CA3 and dentate gyrus (DG)] and amygdala (basolateral/lateral) as well as the BDNF mRNA content in the habenula (medial/lateral). The lesion did not influence BDNF and trkB expression in the caudate-putamen, substantia nigra, nucleus accumbens (shell and core) and ventral tegmental area (VTA). Chronic imipramine reversed the lesion-induced decreases in BDNF mRNA in the DG. Chronic pramipexole increased BDNF mRNA, but decreased trkB mRNA in the VTA in lesioned rats. Furthermore, it reduced BDNF and trkB mRNA expression in the shell and core of the nucleus accumbens, BDNF mRNA in the amygdala and trkB mRNA in the caudate-putamen in these animals. The present study indicates that both the 6-OHDA-induced dopaminergic lesion and chronic pramipexole influence BDNF signalling in limbic structures, which may be related to their pro-depressive and antidepressant activity in rats, respectively.</p></div

The influence of 6-OHDA, pramipexole and imipramine on BDNF and trkB mRNAs in the caudate-putamen.

<p>n = 9–10. For further explanations see Figs. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g002" target="_blank">2</a>.</p

The influence 6-OHDA, pramipexole and imipramine on BDNF and trkB mRNAs in the amygdala.

<p>n = 8–10. For further explanations see Figs. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g002" target="_blank">2</a>.</p

Representative autoradiograms showing BDNF and trkB mRNAs expression in frontal sections of the brain.

<p>Regions of interest are outlined. AMG—amygdala, CP—caudate-putamen, DG—dentate gyrus, HB—habenula, NAC—nucleus accumbens, SN—substantia nigra, VTA—ventral tegmental area. AP—anterior-posterior levels according to Paxinos and Watson [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.ref045" target="_blank">45</a>].</p

The influence of 6-OHDA, pramipexole and imipramine on BDNF and trkB mRNAs in the habenula.

<p>n = 8–10. For further explanations see Figs. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g001" target="_blank">1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0117698#pone.0117698.g002" target="_blank">2</a>.</p