Elevated levels of nausea and vomiting in pregnancy (NVP) and disgust sensitivity have been observed in the first trimester and both are thought to have a protective function for the mother and her fetus. Their aetiology is not clear, however, with previous studies attributing elevated NVP and disgust to various factors including endocrine changes, immunological changes, and psychological variables. To date, no study has directly assessed the relationship between disgust and NVP. Here, we prospectively collected two independent samples (S1 and S2; n1 = 201, n2 = 391) of women in the first trimester of pregnancy, who completed the Index of Nausea, Vomiting, and Retching and the Disgust Scale-Revised. We also measured free β-human chorionic gonadotropin (hCG) and pregnancy-associated plasma protein A (PAPP-A) in maternal serum. Our results did not confirm any association between NVP and disgust; in addition, they indicate that NVP and disgust may have different proximate causes. Disgust sensitivity was significantly negatively correlated with free β-hCG and (only in S1) with PAPP-A. In contrast, NVP was significantly positively associated with free β-hCG levels and (only in S1) with PAPP-A. While low hCG levels seem to be an important indicator for activation of the behavioral immune system in the first trimester, increased hCG levels play a role in stronger symptoms of NVP, a result consistent with previous studies. Levels of PAPP-A are likely part of a larger network of immunological and endocrine responses and do not appear to provide sufficient information for predicting women's NVP and disgust sensitivity.

• MeSH
• biologické markery MeSH
• komplikace těhotenství * MeSH
• lidé MeSH
• lidský choriogonadotropin, beta podjednotka MeSH
• nauzea etiologie   MeSH
• odpor * MeSH
• první trimestr těhotenství MeSH
• těhotenský plazmatický protein A metabolismus   MeSH
• těhotenství MeSH
• zvracení etiologie   MeSH
• Check Tag
• lidé MeSH
• těhotenství MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

• MeSH
• oftalmologické chirurgické výkony metody   MeSH
• oftalmologie dějiny   MeSH
• strabismus dějiny   chirurgie   MeSH

Brain edema accompanying ischemic or traumatic brain injuries, originates from a disruption of ionic/neurotransmitter homeostasis that leads to accumulation of K(+) and glutamate in the extracellular space. Their increased uptake, predominantly provided by astrocytes, is associated with water influx via aquaporin-4 (AQP4). As the removal of perivascular AQP4 via the deletion of α-syntrophin was shown to delay edema formation and K(+) clearance, we aimed to elucidate the impact of α-syntrophin knockout on volume changes in individual astrocytes in situ evoked by pathological stimuli using three dimensional confocal morphometry and changes in the extracellular space volume fraction (α) in situ and in vivo in the mouse cortex employing the real-time iontophoretic method. RT-qPCR profiling was used to reveal possible differences in the expression of ion channels/transporters that participate in maintaining ionic/neurotransmitter homeostasis. To visualize individual astrocytes in mice lacking α-syntrophin we crossbred GFAP/EGFP mice, in which the astrocytes are labeled by the enhanced green fluorescent protein under the human glial fibrillary acidic protein promoter, with α-syntrophin knockout mice. Three-dimensional confocal morphometry revealed that α-syntrophin deletion results in significantly smaller astrocyte swelling when induced by severe hypoosmotic stress, oxygen glucose deprivation (OGD) or 50 mM K(+). As for the mild stimuli, such as mild hypoosmotic or hyperosmotic stress or 10 mM K(+), α-syntrophin deletion had no effect on astrocyte swelling. Similarly, evaluation of relative α changes showed a significantly smaller decrease in α-syntrophin knockout mice only during severe pathological conditions, but not during mild stimuli. In summary, the deletion of α-syntrophin markedly alters astrocyte swelling during severe hypoosmotic stress, OGD or high K(+).

• MeSH
• akvaporin 4 genetika   metabolismus   MeSH
• astrocyty metabolismus   patologie   MeSH
• biologický transport MeSH
• draslík metabolismus   MeSH
• draslíkové kanály genetika   metabolismus   MeSH
• edém mozku genetika   metabolismus   patologie   MeSH
• glukosa nedostatek   MeSH
• konfokální mikroskopie MeSH
• membránové proteiny nedostatek   genetika   MeSH
• mikrotomie MeSH
• mozková kůra metabolismus   patologie   MeSH
• myši transgenní MeSH
• myši MeSH
• osmolární koncentrace MeSH
• osmotický tlak MeSH
• promotorové oblasti (genetika) MeSH
• proteiny nervové tkáně genetika   metabolismus   MeSH
• proteiny vázající vápník nedostatek   genetika   MeSH
• regulace genové exprese MeSH
• signální transdukce MeSH
• stereotaktické techniky MeSH
• svalové proteiny nedostatek   genetika   MeSH
• techniky tkáňových kultur MeSH
• zelené fluorescenční proteiny genetika   metabolismus   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Román, z prostředí české záchranné služby, jehož hlavní hrdinkou je záchranářka.; Kniha z prostředí záchranné služby popisující skutečnou, syrovou realitu práce záchranářů, vzájemných vztahů nejen lékařů, ale i chování pacientů k lékařům i naopak. Knihou se prolíná osobní příběh hlavní hrdinky Jany. Pokračování knihy Ze života peklo.

• MeSH
• interprofesionální vztahy MeSH
• urgentní zdravotnické služby MeSH
• vztahy mezi zdravotnickým pracovníkem a pacientem MeSH
• záchranná práce MeSH
• Publikační typ
• beletrie MeSH
• Geografické názvy
• Česká republika MeSH

• Konspekt
• Česká próza
• NLK Obory
• humanitní vědy a umění

The polymodal transient receptor potential vanilloid 4 (TRPV4) channel, a member of the TRP channel family, is a calcium-permeable cationic channel that is gated by various stimuli such as cell swelling, low pH and high temperature. Therefore, TRPV4-mediated calcium entry may be involved in neuronal and glia pathophysiology associated with various disorders of the central nervous system, such as ischemia. The TRPV4 channel has been recently found in adult rat cortical and hippocampal astrocytes; however, its role in astrocyte pathophysiology is still not defined. In the present study, we examined the impact of cerebral hypoxia/ischemia (H/I) on the functional expression of astrocytic TRPV4 channels in the adult rat hippocampal CA1 region employing immunohistochemical analyses, the patch-clamp technique and microfluorimetric intracellular calcium imaging on astrocytes in slices as well as on those isolated from sham-operated or ischemic hippocampi. Hypoxia/ischemia was induced by a bilateral 15-minute occlusion of the common carotids combined with hypoxic conditions. Our immunohistochemical analyses revealed that 7 days after H/I, the expression of TRPV4 is markedly enhanced in hippocampal astrocytes of the CA1 region and that the increasing TRPV4 expression coincides with the development of astrogliosis. Additionally, adult hippocampal astrocytes in slices or cultured hippocampal astrocytes respond to the TRPV4 activator 4-alpha-phorbol-12,-13-didecanoate (4αPDD) by an increase in intracellular calcium and the activation of a cationic current, both of which are abolished by the removal of extracellular calcium or exposure to TRP antagonists, such as Ruthenium Red or RN1734. Following hypoxic/ischemic injury, the responses of astrocytes to 4αPDD are significantly augmented. Collectively, we show that TRPV4 channels are involved in ischemia-induced calcium entry in reactive astrocytes and thus, might participate in the pathogenic mechanisms of astroglial reactivity following ischemic insult.

• MeSH
• astrocyty fyziologie   MeSH
• DNA primery MeSH
• hipokampus patologie   patofyziologie   MeSH
• imunohistochemie MeSH
• kationtové kanály TRPV fyziologie   MeSH
• krysa rodu rattus MeSH
• metoda terčíkového zámku MeSH
• mozková hypoxie a ischemie patologie   patofyziologie   MeSH
• polymerázová řetězová reakce MeSH
• potkani Wistar MeSH
• sekvence nukleotidů MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Recently, we have identified two astrocytic subpopulations in the cortex of GFAP-EGFP mice, in which the astrocytes are visualized by the enhanced green-fluorescent protein (EGFP) under the control of the human glial fibrillary acidic protein (GFAP) promotor. These astrocytic subpopulations, termed high response- (HR-) and low response- (LR-) astrocytes, differed in the extent of their swelling during oxygen-glucose deprivation (OGD). In the present study we focused on identifying the ion channels or transporters that might underlie the different capabilities of these two astrocytic subpopulations to regulate their volume during OGD. Using three-dimensional confocal morphometry, which enables quantification of the total astrocytic volume, the effects of selected inhibitors of K⁺ and Cl⁻ channels/transporters or glutamate transporters on astrocyte volume changes were determined during 20 minute-OGD in situ. The inhibition of volume regulated anion channels (VRACs) and two-pore domain potassium channels (K(2P)) highlighted their distinct contributions to volume regulation in HR-/LR-astrocytes. While the inhibition of VRACs or K(2P) channels revealed their contribution to the swelling of HR-astrocytes, in LR-astrocytes they were both involved in anion/K⁺ effluxes. Additionally, the inhibition of Na⁺-K⁺-Cl⁻ co-transporters in HR-astrocytes led to a reduction of cell swelling, but it had no effect on LR-astrocyte volume. Moreover, employing real-time single-cell quantitative polymerase chain reaction (PCR), we characterized the expression profiles of EGFP-positive astrocytes with a focus on those ion channels and transporters participating in astrocyte swelling and volume regulation. The PCR data revealed the existence of two astrocytic subpopulations markedly differing in their gene expression levels for inwardly rectifying K⁺ channels (Kir4.1), K(2P) channels (TREK-1 and TWIK-1) and Cl⁻ channels (ClC2). Thus, we propose that the diverse volume changes displayed by cortical astrocytes during OGD mainly result from their distinct expression patterns of ClC2 and K(2P) channels.

• MeSH
• astrocyty cytologie   účinky léků   metabolismus   MeSH
• biologické modely MeSH
• chloridové kanály metabolismus   MeSH
• draslíkové kanály metabolismus   MeSH
• gliový fibrilární kyselý protein metabolismus   MeSH
• glukosa nedostatek   MeSH
• kyslík MeSH
• lidé MeSH
• modulátory membránového transportu farmakologie   MeSH
• mozková kůra cytologie   MeSH
• myši transgenní MeSH
• myši MeSH
• pohlavní dimorfismus MeSH
• regulace genové exprese účinky léků   MeSH
• sodík-draslík-chloridové symportéry metabolismus   MeSH
• stanovení celkové genové exprese MeSH
• symportéry metabolismus   MeSH
• techniky in vitro MeSH
• velikost buňky účinky léků   MeSH
• vezikulární transportní proteiny pro glutamát metabolismus   MeSH
• zelené fluorescenční proteiny metabolismus   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

To understand the structural alterations that underlie early and late changes in hippocampal diffusivity after hypoxia/ischemia (H/I), the changes in apparent diffusion coefficient of water (ADC(W)) were studied in 8-week-old rats after H/I using diffusion-weighted magnetic resonance imaging (DW-MRI). In the hippocampal CA1 region, ADC(W) analyses were performed during 6 months of reperfusion and compared with alterations in cell number/cell-type composition, glial morphology, and extracellular space (ECS) diffusion parameters obtained by the real-time iontophoretic method. In the early phases of reperfusion (1 to 3 days) neuronal cell death, glial proliferation, and developing gliosis were accompanied by an ADC(W) decrease and tortuosity increase. Interestingly, ECS volume fraction was decreased only first day after H/I. In the late phases of reperfusion (starting 1 month after H/I), when the CA1 region consisted mainly of microglia, astrocytes, and NG2-glia with markedly altered morphology, ADC(W), ECS volume fraction and tortuosity were increased. Three-dimensional confocal morphometry revealed enlarged astrocytes and shrunken NG2-glia, and in both the contribution of cell soma/processes to total cell volume was markedly increased/decreased. In summary, the ADC(W) increase in the CA1 region underlain by altered cellular composition and glial morphology suggests that considerable changes in extracellular signal transmission might occur in the late phases of reperfusion after H/I.

• MeSH
• astrocyty patologie   MeSH
• buněčná smrt MeSH
• časové faktory MeSH
• difuze MeSH
• difuzní magnetická rezonance MeSH
• extracelulární prostor metabolismus   MeSH
• glióza etiologie   patologie   MeSH
• hipokampální oblast CA1 patologie   patofyziologie   MeSH
• hypoxie komplikace   patologie   patofyziologie   MeSH
• imunohistochemie MeSH
• ischemie mozku komplikace   patologie   patofyziologie   MeSH
• konfokální mikroskopie MeSH
• krysa rodu rattus MeSH
• neuroglie patologie   MeSH
• počet buněk MeSH
• potkani Wistar MeSH
• proliferace buněk MeSH
• reperfuze MeSH
• tělesná voda metabolismus   MeSH
• zobrazování trojrozměrné MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH

We examined 138 saliva samples for the presence or absence of the blood antigens ABH using haemagglutination inhibition methodology. The outcomes of the tests were scanned and examined by special software, which used the HSV colour model, allowed setting the parameters in a way that enabled differentiation of agglutination clusters from suspensions of erythrocytes and subsequently calculated the area of agglutination clusters. The size of the area was (inversely) related to the presence of ABH substances in saliva. Both the secretor phenotypes and the intensity of secretion into saliva were statistically analysed in relation to gender, blood type, blood group genotype frequencies and secretor genotype frequencies.

• MeSH
• ABO systém krevních skupin analýza   MeSH
• erytrocyty chemie   MeSH
• kolorimetrie MeSH
• lidé MeSH
• mladý dospělý MeSH
• počítačové zpracování obrazu metody   MeSH
• sliny chemie   MeSH
• software MeSH
• testy inhibice hemaglutinace metody   MeSH
• Check Tag
• lidé MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Astrocytes and NG2 glia respond to CNS injury by the formation of a glial scar. Since the changes in K(+) currents in astrocytes and NG2 glia that accompany glial scar formation might influence tissue outcome by altering K(+) ion homeostasis, we aimed to characterize the changes in K(+) currents in hippocampal astrocytes and NG2 glia during an extended time window of reperfusion after ischemic injury. Global cerebral ischemia was induced in adult rats by bilateral, 15-min common carotid artery occlusion combined with low-pressure oxygen ventilation. Using the patch-clamp technique, we investigated the membrane properties of hippocampal astrocytes and NG2 glia in situ 2 hours, 6 hours, 1 day, 3 days, 7 days or 5 weeks after ischemia. Astrocytes in the CA1 region of the hippocampus progressively depolarized starting 3 days after ischemia, which coincided with decreased Kir4.1 protein expression in the gliotic tissue. Other K(+) channels described previously in astrocytes, such as Kir2.1, Kir5.1 and TREK1, did not show any changes in their protein content in the hippocampus after ischemia; however, their expression switched from neurons to reactive astrocytes, as visualized by immunohistochemistry. NG2 glia displayed increased input resistance, decreased membrane capacitance, increased delayed outwardly rectifying and A-type K(+) currents and decreased inward K(+) currents 3 days after ischemia, accompanied by their proliferation. Our results show that the membrane properties of astrocytes after ischemia undergo complex alterations, which might profoundly influence the maintenance of K(+) homeostasis in the damaged tissue, while NG2 glia display membrane currents typical of proliferating cells.

• MeSH
• buněčná membrána metabolismus   patologie   MeSH
• down regulace genetika   fyziologie   MeSH
• draslíkové kanály dovnitř usměrňující antagonisté a inhibitory   biosyntéza   genetika   MeSH
• glióza genetika   metabolismus   patologie   MeSH
• hipokampální oblast CA1 metabolismus   patologie   patofyziologie   MeSH
• ischemie mozku metabolismus   patologie   patofyziologie   MeSH
• krysa rodu rattus MeSH
• membránové potenciály fyziologie   MeSH
• neuroglie metabolismus   patologie   MeSH
• polarita buněk fyziologie   MeSH
• potkani Wistar MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH

Energy depletion during ischemia leads to disturbed ionic homeostasis and accumulation of neuroactive substances in the extracellular space, subsequently leading to volume changes in astrocytes. Confocal microscopy combined with 3D reconstruction was used to quantify ischemia-induced astrocyte volume changes in cortical slices of GFAP/EGFP transgenic mice. Twenty-minutes of oxygen-glucose deprivation (OGD) or oxygen-glucose deprivation combined with acidification (OGD(pH 6.8)) revealed the presence of two distinct astrocytic populations, the first showing a large volume increase (HR astrocytes) and the second displaying a small volume increase (LR astrocytes). In addition, changes in resting membrane potential (V(m)), measured by the patch-clamp technique, supported the existence of two astrocytic populations responding differently to ischemia. Although one group markedly depolarized during OGD or OGD(pH 6.8), only small changes in V(m) toward more negative values were observed in the second group. Conversely, acidification (ACF(pH 6.8)) led to a uniform volume decrease in all astrocytes, accompanied by only a small depolarization. Interestingly, two differently responding populations were not detected during acidification. Differences in the expression of inwardly rectifying potassium channels (Kir4.1), glial fibrillary acidic protein (GFAP), and taurine levels in cortical astrocytes were detected using immunohistochemical methods. We conclude that two distinct populations of astrocytes are present in the cortex of GFAP/EGFP mice, based on volume and V(m) changes during exposure to OGD or OGD(pH 6.8). Immunohistochemical analysis suggests that the diverse expression of Kir4.1 channels and GFAP as well as differences in the accumulation of taurine might contribute to the distinct ability of astrocytes to regulate their volume. 2008 Wiley-Liss, Inc.

• MeSH
• astrocyty fyziologie   klasifikace   patologie   MeSH
• draslíkové kanály dovnitř usměrňující metabolismus   MeSH
• elektrická stimulace MeSH
• financování organizované MeSH
• gliový fibrilární kyselý protein genetika   MeSH
• glukosa nedostatek   MeSH
• hypoxie MeSH
• ischemie patologie   MeSH
• koncentrace vodíkových iontů MeSH
• konfokální mikroskopie MeSH
• membránové potenciály fyziologie   MeSH
• metoda terčíkového zámku MeSH
• modely nemocí na zvířatech MeSH
• mozková kůra patologie   MeSH
• myši transgenní MeSH
• myši MeSH
• proteiny nervové tkáně metabolismus   MeSH
• taurin metabolismus   MeSH
• velikost buňky MeSH
• zelené fluorescenční proteiny genetika   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH