Search

Start Over Format print Data provider Academy of Sciences Library/Knihovna Akademie věd ČR

702. Alois Zucker: jeho vědecká činnost literární a význam její pro vědu práva trestního

Creator:
František Storch
Publisher:
Nákladem vlastním
Format:
print, svazek, and 14 stran.
Type:
model:monograph and TEXT
Subject:
Právo, Zucker, Alois, 1842-1906, 19.-20. století, právníci, 34-051, (437.3), (042.3), 16, and 34
Language:
Czech
Description:
přednáška, kterou měl ve schůzi právnické jednoty v Praze, konané dne 25. října 1906 František Storch.
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

704. Alterations in endothelin receptors following hemorrhage and resuscitation by centhaquin

Creator:
Briyal, S., Gandhakwala, R., Gulati, A., Lavhale, M. S., and Khan, M.
Format:
print, bez média, and svazek
Type:
model:article and TEXT
Subject:
fyziologie člověka, human physiology, Hemorrhagic shock, Centhaquin, Resuscitation, Endothelin, Cytokines, 14, and 612
Language:
English
Description:
Endothelin-1 (ET-1) acts on ETA and ETB receptors and has been implicated in hemorrhagic shock (shock). We determined effect of shock and resuscitation by hypertonic saline (saline) or centhaquin on ETA and ETB receptor expression. Rats were anesthetized, a pressure catheter was placed in the left femoral artery; blood was withdrawn from the right femoral artery to bring mean arterial pressure (MAP) to 35 mm Hg for 30 min, resuscitation was performed and 90 min later sacrificed to collect samples for biochemical estimations. Resuscitation with centhaquin decreased blood lactate and increased MAP. Protein levels of ETA or ETB receptor were unaltered in the brain, heart, lung and liver following shock or resuscitation. In the abdominal aorta, shock produced an increase (140 %) in ETA expression which was attenuated by saline and centhaquin; ETB expression was unaltered following shock but was increased (79 %) by centhaquin. In renal medulla, ETA expression was unaltered following shock, but was decreased (-61 %) by centhaquin; shock produced a decrease (-34 %) in ETB expression which was completely attenuated by centhaquin and not saline. Shock induced changes in ETA and ETB receptors in the aorta and renal medulla are reversed by centhaquin and may be contributing to its efficacy., S. Briyal, R. Gandhakwala, M. Khan, M. S. Lavhale, A. Gulati., and Seznam literatury
Rights:
http://creativecommons.org/publicdomain/mark/1.0/ and policy:public

705. Alterations in the baroreceptor-heart rate reflex in conscious inbred polydipsic (STR/N) mice

Creator:
Chu, C. P., Cui, B. R., Kannan, H., and Qiu, D. L.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, physiology, phenylephrine, sodium nitroprusside, baroreceptor reflex, inbred polydipsic mice, 14, and 612
Language:
English
Description:
STR/N is an inbred strain of mice which is known to exhibit extreme polydipsia and polyuria. We previously found central administration of angiotensin II enhanced cardiovascular responses in STR/N mice than normal mice, suggesting that STR/N mice might exhibit different cardiovascular responses. Therefore, in this study, we investigated daily mean arterial blood pressure and heart rate, and changes in the baroreceptor-heart rate reflex in conscious STR/N mice and control (ICR) mice. We found that variability in daily mean arterial blood pressure and heart rate was significantly larger in STR/N mice than in ICR mice (p<0.05). There was a stronger response to phenylephrine (PE) in STR/N mice than in ICR mice. For baroreceptor reflex sensitivity, in the rapid response period, the slopes of PE and sodium nitroprusside (SNP) were more negative in STR/N mice than in ICR mice. In the later period, the slopes of PE and SNP were negatively correlated between heart rate and blood pressure in ICR mice, but their slopes were positively correlated in STR/N mice. These results indicated that STR/N mice exhibited the different cardiovascular responses than ICR mice, suggesting that the dysfunction of baroreceptor reflex happened in conscious STR/N mice., C. P. Chu, B. R. Cui, H. Kannan, D. L. Qiu., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

706. Alterations in the expression of the apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE/ref-1) and DNA damage in the caudal region of acute and chronic spinal cord injured rats treated by embryonic neural stem cells

Creator:
Dagci, T., Armagan, G., Konyalioglu, S., and Yalcin, A.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, poranění míchy, spinal cord injuries, stem cell transplantation, DNA damage, APE protein, ref-1 protein, 14, and 612
Language:
English
Description:
The oxidative mechanisms of injury-induced damage of neurons within the spinal cord are not very well understood. We used a model of T8-T9 spinal cord injury (SCI) in the rat to induce neuronal degeneration. In this spinal cord injury model, unilateral avulsion of the spinal cord causes oxidative stress of neurons. We tested the hypothesis that apurinic/apyrimidinic endonuclease (or redox effector factor-1, APE/Ref-1) regulates this neuronal oxidation mechanism in the spinal cord region caudal to the lesion, and that DNA damage is an early upstream signal. The embryonic neural stem cell therapy significantly decreased DNA- damage levels in both study groups - acutely (followed up to 7 days after SCI), and chronically (followed up to 28 days after SCI) injured animals. Meanwhile, mRNA levels of APE/Ref-1 significantly increased after embryonic neural stem cell therapy in acutely and chronically injured an imals when compared to acute and chronic sham groups. Our da ta has demonstrated that an increase of APE/Ref-1 mRNA levels in the caudal region of spinal cord strongly correlated with DNA damage after traumatic spinal cord injury. We suggest that DNA damage can be observed both in lesional and caudal regions of the acutely and chronically injured groups, but DNA damage is reduced with embryonic neural stem cell therapy., T. Dagci, G. Armagan, S. Konyalioglu, A. Yalcin., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

707. Alterations of NO synthase isoforms in brain and kidney of rats with genetic and salt hypertension

Creator:
Silvie Hojná, Jaroslav Kuneš, and Jan Zicha
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, ledviny, kidneys, brainstem, diencephalon, NO synthase, genetic hypertension, 14, and 612
Language:
English
Description:
Both brain and peripheral nitric oxide (NO) play a role in the control of blood pressure and circ ulatory homeostasis. Central NO production seems to counteract angiotensin II-induced enhancement of sympathetic tone. The aim of our study was to evaluate NO synthase (NOS) activity and protein expression of its three isoforms - neuronal (nNOS), endothelial NOS (eNOS) and inducible (iNOS) - in two brain regions involved in blood pressure control (diencephalon and brainstem) as well as in the kidney of young adult rats with either genetic (12-week-old SHR) or salt- induced hypertension (8-week-old Dahl rats). We have demonstrated reduced nNOS and iNOS expression in brainstem of both hypertensive models. In SHR this abnormality was accompanied by attenuated NOS activity and was corrected by chronic captopril treatment which prevented the development of genetic hypertension. In salt hypertensive Dahl rats nNOS and iNOS expression was also decrea sed in the diencephalon where neural structures important for salt hypertension development are located. As far as peripheral NOS activity and expression is concerned, renal eNOS expression was considerably reduced in both genetic and salt-induced hypertension. In conclusions, we disclosed similar changes of NO system in the brainstem (but not in the diencephalon) of rats with genetic and salt-induced hypertension. Decreased nNOS ex pression was associated with increased blood pressure due to enhanced sympathetic tone., S. Hojná, J. Kuneš, J. Zicha., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

708. Altered blood-brain barrier permeability and its effect on the distribution of Evans blue and sodium fluorescein in the rat brain applied by intracarotid injection

Creator:
Petr Kozler and Pokorný, J.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, hematoencefalická bariéra, fluorescenční mikroskopie, blood-brain barrier, fluorescence microscopy, cellular edema, intravital dyes, 14, and 612
Language:
English
Description:
The aim was to study the blood-brain permeability according to the distribution in the rat brain of Evans blue (EB) and sodium fluorescein (NaFl) administered by an intracarotid injection. Eighteen animals were divided into six groups according to the state of the blood-brain barrier (BBB) at the moment when the dyes were being applied. In the first two groups, the BBB was intact, in groups 3 and 4 the barrier had been opened osmotically prior to the application of the dyes, and in groups 5 and 6 a cellular edema was induced by hyperhydration before administration of the dyes. The intracellular and extracellular distribution of the dyes was studied by fluorescence microscopy. The histological picture thus represented the morphological correlate of the way BBB permeability had been changed before the application of the dyes., P. Kozler, J. Pokorný., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

709. Altered neural and vascular mechanisms in hypertension

Creator:
Mária Pintérová, Jaroslav Kuneš, and Jiří Zicha
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, bílkoviny, sympatický nervový systém, krevní tlak, proteins, sympathetic nervous system, blood pressure, spontaneously hypertensive rats, alpha- and beta-adrenoceptors, G proteins, L-type voltage-dependent calcium channels, calcium influx, potassium channels, PhoA/Rho-kinase pathway, calcium sensitization, 14, and 612
Language:
English
Description:
b1_Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in th e regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins., b2_ there is considerable information on th e complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing., M. Pintérová, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

710. Altered pulmonary vasoreactivity in the chronically hypoxic lung

Creator:
Shimoda, L. A., Sham, J. S. K., and Sylvester, J. T.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, plicní hypertenze, nitric oxide, pulmonary hypertension, contraction, endothelin-1, angiotensin II, membrane potential, 14, and 612
Language:
English
Description:
Prolonged exposure to alveolar hypoxia induces physiological changes in the pulmonary vasculature that result in the development of pulmonary hypertension. A hallmark of hypoxic pulmonary hypertension is an increase in vasomotor tone. In vivo, pulmonary arterial smooth muscle cell contraction is influenced by vasoconstrictor and vasodilator factors secreted from the endothelium, lung parenchyma and in the circulation. During chronic hypoxia, production of vasoconstrictors such as endothelin-1and angiotensin II is enhanced locally in the lung, while synthesis of vasodilators may be reduced. Altered reactivity to these vasoactive agonists is another physiological consequence of chronic exposure to hypoxia. Enhanced contraction in response to endothelin-1 and angiotensin II, as well as depressed vasodilation in response to endothelium-derived vasodilators, has been documented in models of hypoxic pulmonary hypertension. Chronic hypoxia may also have direct effects on pulmonary vascular smooth muscle cells, modulating receptor population, ion channel activity or signal transduction pathways. Following prolonged hypoxic exposure, pulmonary vascular smooth muscle exhibits alterations in K+ current, membrane depolarization, elevation in resting cytosolic calcium and changes in signal transduction pathways. These changes in the electrophysiological parameters of pulmonary vascular smooth muscle cells are likely associated with an increase in basal tone. Thus, hypoxia-induced modifications in pulmonary arterial myocyte function, changes in synthesis of vasoactive factors and altered vasoresponsiveness to these agents may shift the environment in the lung to one of contraction instead of relaxation, resulting in increased pulmonary vascular resistance and elevated pulmonary arterial pressure., L. A. Shimoda, J. S. K. Sham, J. T. Sylvester., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

Limit your search

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

Show values starting with
more »

View distribution

Current results range from 1480 to 2013

View larger »