Journal articles: 'Centrum prevence'

1

Šedová, Lenka, Vlasta Koudelková, and Věra Adámková. "Centre of Prevention of Civilization Diseases." Kontakt 10, no. 1 (July 27, 2008): 194–99. http://dx.doi.org/10.32725/kont.2008.027.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Haldar, Bikram, Anirban Basu, and Bitan Kumar Chattopadhyay. "Can We Prevent Port Site Infections? Our Experience at a Tertiary Care Centre." New Indian Journal of Surgery 10, no. 5 (2019): 469–73. http://dx.doi.org/10.21088/nijs.0976.4747.10519.2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Rothwell, Nancy J. "Central effects of TNF α on thermogenesis and fever in the rat." Bioscience Reports 8, no. 4 (August 1, 1988): 345–52. http://dx.doi.org/10.1007/bf01115225.

Full text

Abstract:

Intracerebroventricular (icv) injection of purified recombinant human tumour necrosis factor α (TNF α, 4–8μg) in conscious rats, produced increases in colonic temperature (1.0°C) and resting oxygen consumption (VO2, 14%) which were maximal after 80–90 minutes. Pretreatment with propranolol (10mg/kg s.c) significantly inhibited the rise in VO2, and prevented the increase in body temperature. Icv injection of an antagonist to corticotropin releasing factor (α-helical CRF 9–41, 25 μg), which prevents the pyrogenic and thermogenic actions of interleukin-1β, did not influence the effects of TNFα on temperature or VO2. Injection of a fragment of TNFα (113–130 amino acid sequence) did not affect body temperature or VO2. TNFα injection (icv) significantly increased brown adipose tissue (BAT) in vitro mitochondrial GDP binding, and this effect was slightly inhibited, but not prevented, by surgical denervation of the tissue, and was unaffected by pretreatment with α-helical CRF 9–41. These data indicate that TNFα can stimulate thermogenesis by a direct central action. The effects are largely, but not totally, dependent on the sympathetic nervous system but, unlike the thermogenic actions of interleukin they do not require release of CRF.

APA, Harvard, Vancouver, ISO, and other styles

4

Crawley, Brianna, Osamu Saito, Shelle Malkmus, Bethany Fitzsimmons, Xiao-Ying Hua, and Tony L. Yaksh. "Acetaminophen prevents hyperalgesia in central pain cascade." Neuroscience Letters 442, no. 1 (September 2008): 50–53. http://dx.doi.org/10.1016/j.neulet.2008.06.062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Hadaway, Lynn C. "Prevenir la extravasación en una vía central." Nursing (Ed. española) 23, no. 5 (May 2005): 44–45. http://dx.doi.org/10.1016/s0212-5382(05)71426-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Crawley, B. K., S. Malkmus, B. L. Fitzsimmonds, X. Y. Hua, and T. L. Yaksh. "ACETAMINOPHEN PREVENTS HYPERALGESIA IN CENTRAL PAIN CASCADE." Journal of Investigative Medicine 55, no. 1 (January 2007): S101. http://dx.doi.org/10.1097/00042871-200701010-00154.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Huang, Bing S., Roselyn A. White, Arco Y. Jeng, and Frans H. H. Leenen. "Role of central nervous system aldosterone synthase and mineralocorticoid receptors in salt-induced hypertension in Dahl salt-sensitive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R994—R1000. http://dx.doi.org/10.1152/ajpregu.90903.2008.

Full text

Abstract:

In Dahl salt-sensitive (S) rats, high salt intake increases cerebrospinal fluid (CSF) Na+ concentration ([Na+]) and blood pressure (BP). Intracerebroventricular (ICV) infusion of a mineralocorticoid receptor (MR) blocker prevents the hypertension. To assess the role of aldosterone locally produced in the brain, we evaluated the effects of chronic central blockade with the aldosterone synthase inhibitor FAD286 and the MR blocker spironolactone on changes in aldosterone and corticosterone content in the hypothalamus and the increase in CSF [Na+] and hypertension induced by high salt intake in Dahl S rats. After 4 wk of high salt intake, plasma aldosterone and corticosterone were not changed, but hypothalamic aldosterone increased by ∼35% and corticosterone tended to increase in Dahl S rats, whereas both steroids decreased by ∼65% in Dahl salt-resistant rats. In Dahl S rats fed the high-salt diet, ICV infusion of FAD286 or spironolactone did not affect the increase in CSF [Na+]. ICV infusion of FAD286 prevented the increase in hypothalamic aldosterone and 30 mmHg of the 50-mmHg BP increase induced by high salt intake. ICV infusion of spironolactone fully prevented the salt-induced hypertension. These results suggest that, in Dahl S rats, high salt intake increases aldosterone synthesis in the hypothalamus and aldosterone acts as the main MR agonist activating central pathways contributing to salt-induced hypertension.

APA, Harvard, Vancouver, ISO, and other styles

8

Day, Michael. "Failure to monitor independent centres prevents comparison, says watchdog." BMJ 335, no. 7612 (July 26, 2007): 173.1–173. http://dx.doi.org/10.1136/bmj.39283.486551.db.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Nattie, E. E., J. W. Mills, and L. C. Ou. "Pirenzepine prevents diethyl pyrocarbonate inhibition of central CO2 sensitivity." Journal of Applied Physiology 65, no. 5 (November 1, 1988): 1962–66. http://dx.doi.org/10.1152/jappl.1988.65.5.1962.

Full text

Abstract:

Application by pledget of the M1-antimuscarinic receptor agent pirenzepine (40 mM) to the rostral chemosensitive areas of the ventrolateral medulla in anesthetized, paralyzed, vagotomized, glomectomized, and servoventilated cats inhibited the slope of the integrated phrenic response to CO2 by 32.5% (P less than 0.03) and the maximum value by 21.1% (P less than 0.01). Similar application of the imidazole-histidine blocking agent diethyl pyrocarbonate (DEPC) decreased the slope by 40.3% (P less than 0.01) and the maximum value by 29.3% (P less than 0.05). Both responses confirm previous results. DEPC treatment decreased the effectiveness of subsequent pirenzepine application such that although slope and maximum were further decreased, the values were not significantly different from those after DEPC. Pirenzepine treatment prevented any subsequent DEPC inhibitory effect. The results raise the possibility that the inhibitory effects of DEPC on CO2 chemosensitivity are via muscarinic receptors and that muscarinic receptor involvement in CO2 chemosensitivity requires the presence of imidazole-histidine. Analysis by scintillation counting of successive 100-micron sections of medulla after rostral area application of [3H]pirenzepine indicated that the pirenzepine and DEPC effects are most probably within 2.0 mm of the ventral surface as measured from the midline, well away from the dorsal and ventral respiratory group neurons.

APA, Harvard, Vancouver, ISO, and other styles

10

Zivin, J. A. "Cyproheptadine reduces or prevents ischemic central nervous system damage." Neurology 35, no. 4 (April 1, 1985): 584. http://dx.doi.org/10.1212/wnl.35.4.584.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Gabor, Alexander, and Frans H. H. Leenen. "Central neuromodulatory pathways regulating sympathetic activity in hypertension." Journal of Applied Physiology 113, no. 8 (October 15, 2012): 1294–303. http://dx.doi.org/10.1152/japplphysiol.00553.2012.

Full text

Abstract:

The classical neurotransmitters, glutamate and GABA, mediate fast (milliseconds) synaptic transmission and modulate its effectiveness through slow (seconds to minutes) signaling processes. Angiotensinergic pathways, from the lamina terminalis to the paraventricular nucleus (PVN)/supraoptic nucleus and rostral ventrolateral medulla (RVLM), are activated by stimuli such as circulating angiotensin type II (Ang II), cerebrospinal fluid (CSF) sodium ion concentration ([Na+]), and possibly plasma aldosterone, leading to sympathoexcitation, largely by decreasing GABA and increasing glutamate release. The aldosterone-endogenous ouabain (EO) pathway is a much slower neuromodulatory pathway. Aldosterone enhances EO release, and the latter increases chronic activity in angiotensinergic pathways by, e.g., increasing expression for Ang I receptor (AT1R) and NADPH oxidase subunits in the PVN. Blockade of this pathway does not affect the initial sympathoexcitatory and pressor responses but to a large extent, prevents chronic responses to CSF [Na+] or Ang II. Recruitment of these two neuromodulatory pathways allows the central nervous system (CNS) to shift gears to rapidly cause and sustain sympathetic hyperactivity in an efficient manner. Decreased GABA release, increased glutamate release, and enhanced AT1R activation in, e.g., the PVN and RVLM contribute to the elevated blood pressure in a number of hypertension models. In Dahl S rats and spontaneous hypertensive rats, high salt activates the CNS aldosterone-EO pathway, and the salt-induced hypertension can be prevented/reversed by specific CNS blockade of any of the steps in the cascade from aldosterone synthase to AT1R. Further studies are needed to advance our understanding of how and where in the brain these rapid, slow, and very slow CNS pathways are activated and interact in models of hypertension and other disease states associated with chronic sympathetic hyperactivity.

APA, Harvard, Vancouver, ISO, and other styles

12

Delgado, Tia J., Mohamed A. R. Arbab, Evald Rosengren, and Niels-Aage Svendgaard. "Effect of Neonatal 6-Hydroxydopamine Treatment on Experimental Vasospasm following a Subarachnoid Hemorrhage in the Rat." Journal of Cerebral Blood Flow & Metabolism 7, no. 3 (June 1987): 289–94. http://dx.doi.org/10.1038/jcbfm.1987.65.

Full text

Abstract:

Intracisternal injection of blood in the rat produces an angiographically demonstrable biphasic cerebral arterial vasospasm. Systemic 6-hydroxydopamine (6-OHDA) treatment in the neonatal stage, which causes a depletion of noradrenaline (NA) from both sympathetic and central NA-containing nerve fibers, prevents the development of the late spasm phase, while the acute spasm occurs to the same extent as in normal animals. The occurrence of acute spasm can be prevented by lesioning in the mesencephalon of the ascending catecholamine fibers originating in the lower brainstem and projecting to the hypothalamus. It is suggested that 6-OHDA treatment results in the altered spasm pattern via its effect on catecholamine fibers projecting between the medullary A1 and A2 nuclei and the hypothalamus. The occurrence of acute but not late spasm indicates that there is a different pathway underlying the two spasm phases.

APA, Harvard, Vancouver, ISO, and other styles

13

Donnelly, Sandra M., Jannet T. Huang, Xiaopeng P. Zhou, and Catharine I. Whiteside. "Prevention of early glomerulopathy with tolrestat in the streptozotocin-induced diabetic rat." Biochemistry and Cell Biology 74, no. 3 (May 1, 1996): 355–62. http://dx.doi.org/10.1139/o96-038.

Full text

Abstract:

Hyperglycemia is of central importance in the pathogenesis of the complications of diabetes mellitus. Glucose activation of the polyol pathway may lead to renal arteriolar smooth muscle and glomerular mesangial cell hypocontractility. In the streptozotocin-induced diabetic rat, the effect of the aldose reductase inhibitor, tolrestat, in preventing glomerular hyperfiltration, renal hypertrophy, extracellular matrix accumulation, and mesangial cell hypocontractility was addressed. Streptozotocin-induced diabetic rats were followed for 12 weeks and half received tolrestat (25 mg/kg per day). Increased glomerular filtration rate was prevented by tolrestat (3.1 ± 0.3 vs. 1.8 ± 0.2 mL/min, diabetes vs. diabetes + tolrestat, p < 0.01), in part by reduction of the filtration fraction (0.39 ± 0.03 vs. 0.29 ± 0.01, diabetes vs. diabetes + tolrestat, p < 0.01). Tolrestat prevented the raised albumin excretion rates (3594 ± 1154 vs. 713 ± 161 mg/24 h, diabetes vs. diabetes + tolrestat, p < 0.01). Endothelin-1-induced contraction of isolated glomeruli was normal in tolrestat-treated diabetic animals compared with the hypocontractile diabetic glomeruli. Tolrestat prevented glomerular hypertrophy (1.86 ± 0.10 vs. 1.49 ± 0.03 μm2 × 105, diabetes vs. diabetes + tolrestat, p < 0.001) and attenuated the accumulation of basement-membrane-like material (50.2 ± 0.4% vs. 46.4 ± 0.8%, diabetes vs. diabetes + tolrestat, p < 0.001). Fractional mesangial expansion was unchanged in tolrestat-treated diabetic rats compared with untreated animals. Tolrestat prevents the functional changes of glomerular hyperfiltration, mesangial cell hypocontractility, and increased glomerular permeability to albumin. Polyol accumulation may have differential effects on glomerular growth and extracellular matrix accumulation in early diabetic nephropathy.Key words: aldose reductase, nephropathy, renal hemodynamics, renal morphometry, mesangium.

APA, Harvard, Vancouver, ISO, and other styles

14

Klarr, S. A., R. F. Keep, and A. L. Betz. "Chronic central potassium infusion prevents deoxycorticosterone-salt hypertension in rats." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H646—H652. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h646.

Full text

Abstract:

Although it has long been established that cerebrospinal fluid potassium concentration (CSF [K]) is very tightly regulated, it has been reported that rats made hypertensive by central infusions of aldosterone have significantly lower CSF [K] compared with normotensive controls. We investigated whether reduced CSF [K] is also present in another animal model of hypertension, the deoxycorticosterone acetate (DOCA)-salt rat, and we hypothesized that chronic intracerebroventricular (IVT) infusion of potassium with miniosmotic pumps might attenuate the rise in blood pressure observed in these rats. DOCA-salt rats without IVT infusions or with control CSF infusions (0.5 microliter/h of 2.9 mM K for 2 wk) had a significantly increased systolic blood pressure and a significantly lower CSF [K] compared with their respective sham groups. In contrast, DOCA-salt rats receiving IVT infusions with elevated [K] (10, 30, or 150 mM) had significantly lower blood pressures compared with those receiving control CSF. They also did not exhibit decreased CSF [K] compared with their respective sham groups. At 10 and 150 mM K, the blood pressure rise in DOCA-salt rats was not significantly different from shams. At 30 mM K, there was a slight, but significant, increase in blood pressure in the DOCA-salt rats compared with their shams, but this rise was still much less than in DOCA-salt rats infused with 2.9 mM K. Infusions with elevated [K] had no effect on blood pressure in the sham animals. These studies suggest that altered brain potassium homeostasis may play an important role in the development of DOCA-salt hypertension.

APA, Harvard, Vancouver, ISO, and other styles

15

Scrogin, Karie E., Roland Veelken, and Alan Kim Johnson. "Central methysergide prevents renal sympathoinhibition and bradycardia during hypotensive hemorrhage." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 1 (January 1, 1998): H43—H51. http://dx.doi.org/10.1152/ajpheart.1998.274.1.h43.

Full text

Abstract:

Mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were measured in conscious rats during either hemorrhage or cardiopulmonary chemoreceptor stimulation with phenylbiguanide (PBG) after intracerebroventricular injection of the 5-HT1/5-HT2-receptor antagonist, methysergide (40 μg). Progressive hemorrhage caused an initial rise (109 ± 33%) followed by a fall in RSNA (−60 ± 7%) and a fall in HR (−126 ± 7 beats/min). Methysergide delayed the hypotension and prevented both the sympathoinhibitory and bradycardic responses to hemorrhage. Systemic 5-HT3-receptor blockade did not influence responses to hemorrhage. The PBG infusion caused transient depressor (−25 ± 6 mmHg), bradycardic (−176 ± 40 beats/min), and renal sympathostimulatory (182 ± 47% baseline) responses that were not affected by central methysergide (−20 ± 6 mmHg, −162 ± 18 beats/min, 227 ± 46% baseline). These data indicate that a central serotonergic receptor-mediated component contributes to the sympathoinhibitory and bradycardic responses to hypotensive hemorrhage in conscious rats. Furthermore, the same central 5-HT-receptor populations involved in reflex responses to hypotensive hemorrhage probably do not mediate the sympathoinhibitory response to cardiopulmonary chemosensitive 5-HT3 receptors.

APA, Harvard, Vancouver, ISO, and other styles

16

Wilkinson, M. F., and N. W. Kasting. "Central vasopressin V1-blockade prevents salicylate but not acetaminophen antipyresis." Journal of Applied Physiology 68, no. 5 (May 1, 1990): 1793–98. http://dx.doi.org/10.1152/jappl.1990.68.5.1793.

Full text

Abstract:

Recent evidence has suggested that the endogenous antipyretic arginine vasopressin (AVP) may participate in drug-induced antipyresis. This study sought to further those investigations by comparing the effects of two other antipyretic drugs, sodium salicylate and acetaminophen, administered intraperitoneally, during AVP V1-receptor blockade within the ventral septal area (VSA) of the rat brain. During endotoxin-evoked fever, V1-receptor blockade within the VSA of the conscious unrestrained rat significantly antagonized the antipyretic effects of salicylate. The effects of the V1-antagonist on salicylate-induced antipyresis were dose related. In contrast, the antipyresis elicited by acetaminophen was unaffected by VSA V1-antagonist pretreatment. Neither saline nor the V1-antagonist microinjected into the VSA of febrile or nonfebrile rats had any significant effects on the normal progression of endotoxin fever or normal core temperature, respectively. These data suggest that the mechanism of action of salicylate-induced antipyresis includes activation of AVP V1-type receptors within the VSA, as has been shown for indomethacin. However, the lack of effect of the V1-antagonist on antipyresis induced by acetaminophen indicates that not all antipyretic drugs act through the same mechanism in the brain.

APA, Harvard, Vancouver, ISO, and other styles

17

Park, Jang-June, Ryusuke Omiya, Yumiko Matsumura, Yukimi Sakoda, Atsuo Kuramasu, Mathew M. Augustine, Sheng Yao, et al. "B7-H1/CD80 interaction is required for the induction and maintenance of peripheral T-cell tolerance." Blood 116, no. 8 (August 26, 2010): 1291–98. http://dx.doi.org/10.1182/blood-2010-01-265975.

Full text

Abstract:

Abstract T-cell tolerance is the central program that prevents harmful immune responses against self-antigens, in which inhibitory PD-1 signal given by B7-H1 interaction plays an important role. Recent studies demonstrated that B7-H1 binds CD80 besides PD-1, and B7-H1/CD80 interaction also delivers inhibitory signals in T cells. However, a role of B7-H1/CD80 signals in regulation of T-cell tolerance has yet to be explored. We report here that attenuation of B7-H1/CD80 signals by treatment with anti–B7-H1 monoclonal antibody, which specifically blocks B7-H1/CD80 but not B7-H1/PD-1, enhanced T-cell expansion and prevented T-cell anergy induction. In addition, B7-H1/CD80 blockade restored Ag responsiveness in the previously anergized T cells. Experiments using B7-H1 or CD80-deficient T cells indicated that an inhibitory signal through CD80, but not B7-H1, on T cells is responsible in part for these effects. Consistently, CD80 expression was detected on anergic T cells and further up-regulated when they were re-exposed to the antigen (Ag). Finally, blockade of B7-H1/CD80 interaction prevented oral tolerance induction and restored T-cell responsiveness to Ag previously tolerized by oral administration. Taken together, our findings demonstrate that the B7-H1/CD80 pathway is a crucial regulator in the induction and maintenance of T-cell tolerance.

APA, Harvard, Vancouver, ISO, and other styles

18

Schiavone, Stefania, Paolo Tucci, Luigia Trabace, and Maria Grazia Morgese. "Early Celastrol Administration Prevents Ketamine-Induced Psychotic-Like Behavioral Dysfunctions, Oxidative Stress and IL-10 Reduction in The Cerebellum of Adult Mice." Molecules 24, no. 21 (November 5, 2019): 3993. http://dx.doi.org/10.3390/molecules24213993.

Full text

Abstract:

Administration of subanesthetic doses of ketamine during brain maturation represents a tool to mimic an early insult to the central nervous system (CNS). The cerebellum is a key player in psychosis pathogenesis, to which oxidative stress also contributes. Here, we investigated the impact of early celastrol administration on behavioral dysfunctions in adult mice that had received ketamine (30 mg/kg i.p.) at postnatal days (PNDs) 7, 9, and 11. Cerebellar levels of 8-hydroxydeoxyguanosine (8-OHdG), NADPH oxidase (NOX) 1 and NOX2, as well as of the calcium-binding protein parvalbumin (PV), were also assessed. Furthermore, celastrol effects on ketamine-induced alterations of proinflammatory (TNF-α, IL-6 and IL-1β) and anti-inflammatory (IL-10) cytokines in this brain region were evaluated. Early celastrol administration prevented ketamine-induced discrimination index decrease at adulthood. The same was found for locomotor activity elevations and increased close following and allogrooming, whereas no beneficial effects on sniffing impairment were detected. Ketamine increased 8-OHdG in the cerebellum of adult mice, which was also prevented by early celastrol injection. Cerebellar NOX1 levels were enhanced at adulthood following postnatal ketamine exposure. Celastrol per se induced NOX1 decrease in the cerebellum. This effect was more significant in animals that were early administered with ketamine. NOX2 levels did not change. Ketamine administration did not affect PV amount in the cerebellum. TNF-α levels were enhanced in ketamine-treated animals; however, this was not prevented by early celastrol administration. While no changes were observed for IL-6 and IL-1β levels, ketamine determined a reduction of cerebellar IL-10 expression, which was prevented by early celastrol treatment. Our results suggest that NOX inhibition during brain maturation prevents the development of psychotic-like behavioral dysfunctions, as well as the increased cerebellar oxidative stress and the reduction of IL-10 in the same brain region following ketamine exposure in postnatal life. This opens novel neuroprotective opportunities against early detrimental insults occurring during brain development.

APA, Harvard, Vancouver, ISO, and other styles

19

Huang, Bing S., Roselyn A. White, Monir Ahmad, Arco Y. Jeng, and Frans H. H. Leenen. "Central infusion of aldosterone synthase inhibitor prevents sympathetic hyperactivity and hypertension by central Na+ in Wistar rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 1 (July 2008): R166—R172. http://dx.doi.org/10.1152/ajpregu.90352.2008.

Full text

Abstract:

In Wistar rats, increasing cerebrospinal fluid (CSF) Na+ concentration ([Na+]) by intracerebroventricular (ICV) infusion of hypertonic saline causes sympathetic hyperactivity and hypertension that can be prevented by blockade of brain mineralocorticoid receptors (MR). To assess the role of aldosterone produced locally in the brain in the activation of MR in the central nervous system (CNS), Wistar rats were infused ICV with artificial CSF (aCSF), Na+-rich (800 mmol/l) aCSF, aCSF plus the aldosterone synthase inhibitor FAD286 (100 μg·kg−1·day−1), or Na+-rich aCSF plus FAD286. After 2 wk of infusion, rats treated with Na+-rich aCSF exhibited significant increases in aldosterone and corticosterone content in the hypothalamus but not in the hippocampus, as well as increases in resting blood pressure (BP) and sympathoexcitatory responses to air stress, and impairment of arterial baroreflex function. Concomitant ICV infusion of FAD286 prevented the Na+-induced increase in hypothalamic aldosterone but not corticosterone and prevented most of the increases in resting BP and sympathoexcitatory and pressor responses to air stress and the baroreflex impairment. FAD286 had no effects in rats infused with ICV aCSF. In another set of rats, 24-h BP and heart rate were recorded via telemetry before and during a 14-day ICV infusion of Na+-rich aCSF with or without FAD286. Na+-rich aCSF without FAD286 caused sustained increases (∼10 mmHg) in resting mean arterial pressure that were absent in the rats treated with FAD286. These data suggest that in Wistar rats, an increase in CSF [Na+] may increase the biosynthesis of corticosterone and aldosterone in the hypothalamus, and mainly aldosterone activates MR in the CNS leading to sympathetic hyperactivity and hypertension.

APA, Harvard, Vancouver, ISO, and other styles

20

Bonzón-Kulichenko, Elena, Dominik Schwudke, Nilda Gallardo, Eduardo Moltó, Teresa Fernández-Agulló, Andrej Shevchenko, and Antonio Andrés. "Central Leptin Regulates Total Ceramide Content and Sterol Regulatory Element Binding Protein-1C Proteolytic Maturation in Rat White Adipose Tissue." Endocrinology 150, no. 1 (September 18, 2008): 169–78. http://dx.doi.org/10.1210/en.2008-0505.

Full text

Abstract:

Obesity and type 2 diabetes are associated with insulin and leptin resistance, and increased ceramide contents in target tissues. Because the adipose tissue has become a central focus in these diseases, and leptin-induced increases in insulin sensitivity may be related to effects of leptin on lipid metabolism, we investigated herein whether central leptin was able to regulate total ceramide levels and the expression of enzymes involved in ceramide metabolism in rat white adipose tissue (WAT). After 7 d central leptin treatment, the total content of ceramides was analyzed by quantitative shotgun lipidomics mass spectrometry. The effects of leptin on the expression of several enzymes of the sphingolipid metabolism, sterol regulatory element binding protein (SREBP)-1c, and insulin-induced gene 1 (INSIG-1) in this tissue were studied. Total ceramide levels were also determined after surgical WAT denervation. Central leptin infusion significantly decreased both total ceramide content and the long-chain fatty acid ceramide species in WAT. Concomitant with these results, leptin decreased the mRNA levels of enzymes involved in de novo ceramide synthesis (SPT-1, LASS2, LASS4) and ceramide production from sphingomyelin (SMPD-1/2). The mRNA levels of enzymes of ceramide degradation (Asah1/2) and utilization (sphingomyelin synthase, ceramide kinase, glycosyl-ceramide synthase, GM3 synthase) were also down-regulated. Ceramide-lowering effects of central leptin were prevented by local autonomic nervous system denervation of WAT. Finally, central leptin treatment markedly increased INSIG-1 mRNA expression and impaired SREBP-1c activation in epididymal WAT. These observations indicate that in vivo central leptin, acting through the autonomic nervous system, regulates total ceramide levels and SREBP-1c proteolytic maturation in WAT, probably contributing to improve the overall insulin sensitivity. Central leptin decreases total ceramide levels and prevents sterol regulatory element binding protein (SREBP-1C) proteolytic maturation in white adipose tissue, and probably, in this way, contributes to improve the overall insulin sensitivity.

APA, Harvard, Vancouver, ISO, and other styles

21

Mejía-Vilet, Juan M., Victoria Ramírez, Cristino Cruz, Norma Uribe, Gerardo Gamba, and Norma A. Bobadilla. "Renal ischemia-reperfusion injury is prevented by the mineralocorticoid receptor blocker spironolactone." American Journal of Physiology-Renal Physiology 293, no. 1 (July 2007): F78—F86. http://dx.doi.org/10.1152/ajprenal.00077.2007.

Full text

Abstract:

Renal ischemia and reperfusion (I/R) injury is the major cause of acute renal failure and may also be involved in the development and progression of some forms of chronic kidney disease. We previously showed that a mineralocorticoid receptor (MR) blockade prevents renal vasoconstriction induced by cyclosporine that leads to acute and chronic renal failure (Feria I, Pichardo I, Juarez P, Ramirez V, Gonzalez MA, Uribe N, Garcia-Torres R, Lopez-Casillas F, Gamba G, Bobadilla NA. Kidney Int 63: 43–52, 2003; Perez-Rojas JM, Derive S, Blanco JA, Cruz C, Martinez de la Maza L, Gamba G, Bobadilla NA. Am J Physiol Renal Physiol 289: F1020–F1030, 2005). Thus we investigated whether spironolactone administration prevents the functional and structural damage induced by renal ischemia-reperfusion (I/R). Five groups were studied: sham-operated animals, rats that underwent 20 min of ischemia and 24 h of reperfusion, and three groups that received spironolactone 1, 2, or 3 days before I/R, respectively. Renal I/R produced significant renal dysfunction and tubular damage. Spironolactone administration completely prevented a decrease in renal blood flow, the development of acute renal failure, and tubular apoptosis. The protection conferred by spironolactone was characterized by decreasing oxidative stress, as evidenced by a reduction in kidney lipoperoxidation, increasing expression of antioxidant enzymes, and restoration of urinary NO2/NO3 excretion. Endothelial nitric oxide synthase expression was upregulated by a mineralocorticoid receptor blockade in I/R groups; in addition, an increase in activating phosphorylation of this enzyme at residue S1177 and a decrease in inactivating phosphorylation at T497 were observed. In conclusion, our study shows that spironolactone administration prevents the renal injury induced by I/R, suggesting that aldosterone plays a central role in this model of renal injury.

APA, Harvard, Vancouver, ISO, and other styles

22

Hurt, Ryan T., Paul J. Matheson, Jason W. Smith, El Rasheid Zakaria, Saad P. Shaheen, Craig J. McClain, and R. Neal Garrison. "Preservation of hepatic blood flow by direct peritoneal resuscitation improves survival and prevents hepatic inflammation following hemorrhagic shock." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 10 (November 15, 2012): G1144—G1152. http://dx.doi.org/10.1152/ajpgi.00278.2011.

Full text

Abstract:

Conventional resuscitation (CR) from hemorrhagic shock (HS) results in gut and liver hypoperfusion, organ and cellular edema, and vital organ injury. Adjunct direct peritoneal resuscitation (DPR) with dialysate prevents gut vasoconstriction, hypoperfusion, and injury. We hypothesized that DPR might also improve hepatocellular edema, inflammation, and injury. Anesthetized male SD rats were assigned to groups ( n = 8/group): 1) sham (no HS); 2) HS (40% MAP/60 min) + intravenous fluid conventional resuscitation [CR; shed blood + 2 vol saline (SAL)/30 min]; 3) HS+CR+DPR (30 ml ip 2.5% glucose dialysate); or 4) HS+CR+SAL (30 ml ip saline). Histopathology showed lung and liver injury in HS+CR and HS+CR+SAL up to 24-h postresuscitation (post-RES) that was not in shams and which was prevented by adjunct DPR. Wet-to-dry weight ratios in HS+CR revealed organ edema formation that was prevented by adjunct DPR. HS+CR and HS+CR+SAL had 34% mortality by 24-h post-RES, which was absent with DPR (0%). Liver IFN-γ and IL-6 levels were elevated in CR compared with DPR or shams. TNF-α mRNA was upregulated in CR/sham and DPR/sham. IL-17 was downregulated in DPR/sham. CXCL10 mRNA was upregulated in CR/sham but downregulated in DPR/sham. Despite restored central hemodynamic performance after CR of HS, liver blood flow was compromised up to 24 h post-RES, and the addition of DPR restores and maintains liver perfusion at 24-h post-RES. DPR prevented liver injury, histological damage, and edema formation compared with CR alone. DPR provided a mitigating anti-inflammatory dampening of the systemic inflammatory response. In all, these effects likely account for improved survivorship in the DPR-treated group.

APA, Harvard, Vancouver, ISO, and other styles

23

Nguyen, Trang T. T., Rebecca A. Elsner, and Nicole Baumgarth. "Natural IgM Prevents Autoimmunity by Enforcing B Cell Central Tolerance Induction." Journal of Immunology 194, no. 4 (January 16, 2015): 1489–502. http://dx.doi.org/10.4049/jimmunol.1401880.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Boyer, Nelly, Jérémy Signoret-Genest, Alain Artola, Radhouane Dallel, and Lénaïc Monconduit. "Propranolol treatment prevents chronic central sensitization induced by repeated dural stimulation." PAIN 158, no. 10 (October 2017): 2025–34. http://dx.doi.org/10.1097/j.pain.0000000000001007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Hermes, M. L., R. M. Buijs, M. Masson-Pevet, T. P. van der Woude, P. Pevet, R. Brenkle, and R. Kirsch. "Central vasopressin infusion prevents hibernation in the European hamster (Cricetus cricetus)." Proceedings of the National Academy of Sciences 86, no. 16 (August 1, 1989): 6408–11. http://dx.doi.org/10.1073/pnas.86.16.6408.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Rawish, Elias, Laura Nickel, Franziska Schuster, Ines Stölting, Alex Frydrychowicz, Kathrin Saar, Norbert Hübner, Alaa Othman, Lars Kuerschner, and Walter Raasch. "Telmisartan prevents development of obesity and normalizes hypothalamic lipid droplets." Journal of Endocrinology 244, no. 1 (January 2020): 95–110. http://dx.doi.org/10.1530/joe-19-0319.

Full text

Abstract:

The AT1 receptor blocker telmisartan (TEL) prevents diet-induced obesity. Hypothalamic lipid metabolism is functionally important for energy homeostasis, as a surplus of lipids induces an inflammatory response in the hypothalamus, thus promoting the development of central leptin resistance. However, it is unclear as to whether TEL treatment affects the lipid status in the hypothalamus. C57BL/6N mice were fed with chow (CONchow) or high-fat diet (CONHFD). HFD-fed mice were gavaged with TEL (8 mg/kg/day, 12 weeks, TELHFD). Mice were phenotyped regarding weight gain, energy homeostasis, and glucose control. Hypothalamic lipid droplets were analyzed by fluorescence microscopy. Lipidomics were assessed by performing liquid chromatography-mass spectrometry in plasma and hypothalami. Adipokines were investigated using immunosorbent assays. Glial fibrillary acidic protein (GFAP) was determined by Western blotting and immunohistochemical imaging. We found that body weight, energy homeostasis, and glucose control of TEL-treated mice remained normal while CONHFD became obese. Hypothalamic ceramide and triglyceride levels as well as alkyne oleate distribution were normalized in TELHFD. The lipid droplet signal in the tanycyte layer was higher in CONHFD than in CONchow and returned to normal under TELHFD conditions. High hypothalamic levels of GFAP protein indicate astrogliosis of CONHFD mice while normalized GFAP, TNFα, and IL1α levels of TELHFD mice suggest that TEL prevents hypothalamic inflammation. In conclusion, TEL has anti-obese efficacy and prevented lipid accumulation and lipotoxicity, which is accompanied by an anti-inflammatory effect in the murine hypothalamus. Our findings support the notion that a brain-related mechanism is involved in TEL-induced weight loss.

APA, Harvard, Vancouver, ISO, and other styles

27

Hsieh, Ya-Ching, Michael Frink, Chi-Hsun Hsieh, Mashkoor A. Choudhry, Martin G. Schwacha, Kirby I. Bland, and Irshad H. Chaudry. "Downregulation of migration inhibitory factor is critical for estrogen-mediated attenuation of lung tissue damage following trauma-hemorrhage." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 5 (May 2007): L1227—L1232. http://dx.doi.org/10.1152/ajplung.00479.2006.

Full text

Abstract:

Although studies have shown that 17β-estradiol (E2) prevents neutrophil infiltration and organ damage following trauma-hemorrhage, the mechanism by which E2inhibits neutrophil transmigration remains unknown. Macrophage migration inhibitory factor (MIF) is thought to play a central role in exacerbation of inflammation and is associated with lung injury. MIF regulates the inflammatory response through modulation of Toll-like receptor 4 (TLR4). Activation of TLR4 results in the release of proinflammatory cytokines and chemokines, which induce neutrophil infiltration and subsequent tissue damage. We hypothesized that E2mediates its salutary effects in the lung following trauma-hemorrhage via negative regulation of MIF and modulation of TLR4 and cytokine-induced chemotaxis. C3H/HeOuJ mice were subjected to trauma-hemorrhage (mean blood pressure 35 ± 5 mmHg for ∼90 min, then resuscitation) or sham operation. Mice received vehicle, E2, or E2in combination with recombinant mouse MIF protein (rMIF). Trauma-hemorrhage increased lung MIF and TLR4 protein levels as well as lung and systemic levels of cytokines/chemokines. Treatment of animals with E2following trauma-hemorrhage prevented these changes. However, administration of rMIF protein with E2abolished the E2-mediated decrease in lung TLR4 levels, lung and plasma levels of IL-6, TNF-α, monocyte chemoattractant protein-1, and keratinocyte-derived chemokine (KC). Administration of rMIF protein also prevented E2-mediated reduction in neutrophil influx and tissue damage in the lungs following trauma-hemorrhage. These results suggest that the protective effects of E2on lung injury following trauma-hemorrhage are mediated via downregulation of lung MIF and TLR4-induced cytokine/chemokine production.

APA, Harvard, Vancouver, ISO, and other styles

28

Rana, Abdul Qayyum, Afshan Rana, and Sohaib Mohammad. "Can central pontine myelinolysis be prevented through non-rapid serum sodium correction?" Acta Neurologica Belgica 113, no. 3 (October 12, 2012): 341–42. http://dx.doi.org/10.1007/s13760-012-0141-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Chu, Ruby Z. "Prevenir las caídas de pacientes hospitalizados: el papel central de la enfermera." Nursing (Ed. española) 34, no. 6 (November 2017): 20–25. http://dx.doi.org/10.1016/j.nursi.2017.11.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Cabral, Antonio Melo, Ilce Ferreira da Silva, Catia Rocha Gardioli, and Rubia Grecco Menegaz. "Chronic activation of central α2-adrenoceptors prevents hypertension in DOCA-salt rats." Autonomic Neuroscience 82, no. 3 (August 2000): 146–53. http://dx.doi.org/10.1016/s0165-1838(00)00093-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Arenas, Ernest, and Hakan Persson. "Neurotrophin-3 prevents the death of adult central noradrenergic neurons in vivo." Nature 367, no. 6461 (January 1994): 368–71. http://dx.doi.org/10.1038/367368a0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Wilcox, Barbara J., Michael D. Applegate, Carlos Portera-Cailliau, and Vassilis E. Koliatsos. "Nerve growth factor prevents apoptotic cell death in injured central cholinergic neurons." Journal of Comparative Neurology 359, no. 4 (September 4, 1995): 573–85. http://dx.doi.org/10.1002/cne.903590405.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Habibi-Asl, Bohlool, Kambiz Hassanzadeh, and Mohammad Charkhpour. "Central Administration of Minocycline and Riluzole Prevents Morphine-Induced Tolerance in Rats." Anesthesia & Analgesia 109, no. 3 (September 2009): 936–42. http://dx.doi.org/10.1213/ane.0b013e3181ae5f13.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Harding, Chelsea. "Adult Bone Marrow Transplant Unit Significantly Prevents Central Line-Associated Bloodstream Infections." Biology of Blood and Marrow Transplantation 25, no. 3 (March 2019): S426. http://dx.doi.org/10.1016/j.bbmt.2018.12.484.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Haarbo, Jens, Ulla Marslew, Anders Gotfredsen, and Claus Christiansen. "Postmenopausal hormone replacement therapy prevents central distribution of body fat after menopause." Metabolism 40, no. 12 (December 1991): 1323–26. http://dx.doi.org/10.1016/0026-0495(91)90037-w.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Wang, Chaoran, Mateusz Ruszkowski, and H.-Y. Karen Yang. "Chaotic cold accretion in giant elliptical galaxies heated by AGN cosmic rays." Monthly Notices of the Royal Astronomical Society 493, no. 3 (February 26, 2020): 4065–76. http://dx.doi.org/10.1093/mnras/staa550.

Full text

Abstract:

ABSTRACT Black hole feedback plays a central role in shaping the circumgalactic medium (CGM) of elliptical galaxies. We systematically study the impact of plasma physics on the evolution of ellipticals by performing three-dimensional non-ideal magnetohydrodynamic simulations of the interactions of active galactic nucleus (AGN) jets with the CGM including magnetic fields, and cosmic rays (CRs) and their transport processes. We find that the physics of feedback operating on large galactic scales depends very sensitively on plasma physics operating on small scales. Specifically, we demonstrate that (i) in the purely hydrodynamical case, the AGN jets initially maintain the atmospheres in global thermal balance. However, local thermal instability generically leads to the formation of massive cold discs in the vicinity of the central black hole in disagreement with observations; (ii) including weak magnetic fields prevents the formation of the discs because local B-field amplification in the precipitating cold gas leads to strong magnetic breaking, which quickly extracts angular momentum from the accreting clouds. The magnetic fields transform the cold clouds into narrow filaments that do not fall ballistically; (iii) when plasma composition in the AGN jets is dominated by CRs, and CR transport is neglected, the atmospheres exhibit cooling catastrophes due to inefficient heat transfer from the AGN to CGM despite Coulomb/hadronic CR losses being present; (iv) including CR streaming and heating restores agreement with the observations, i.e. cooling catastrophes are prevented and massive cold central discs do not form. The AGN power is reduced as its energy is utilized efficiently.

APA, Harvard, Vancouver, ISO, and other styles

37

Huang, Bing S., Roselyn A. White, Li Bi, and Frans H. H. Leenen. "Central infusion of aliskiren prevents sympathetic hyperactivity and hypertension in Dahl salt-sensitive rats on high salt intake." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 7 (April 1, 2012): R825—R832. http://dx.doi.org/10.1152/ajpregu.00368.2011.

Full text

Abstract:

Central infusion of an angiotensin type 1 (AT1) receptor blocker prevents sympathetic hyperactivity and hypertension in Dahl salt-sensitive (S) rats on high salt. In the present study, we examined whether central infusion of a direct renin inhibitor exerts similar effects. Intracerebroventricular infusion of aliskiren at the rate of 0.05 mg/day markedly inhibited the increase in ANG II levels in the cerebrospinal fluid and in blood pressure (BP) caused by intracerebroventricular infusion of rat renin. In Dahl S rats on high salt, intracerebroventricular infusion of aliskiren at 0.05 and 0.25 mg/day for 2 wk similarly decreased resting BP in Dahl S rats on high salt. In other groups of Dahl S rats, high salt intake for 2 wk increased resting BP by ∼25 mmHg, enhanced pressor and sympathoexcitatory responses to air-stress, and desensitized arterial baroreflex function. All of these effects were largely prevented by intracerebroventricular infusion of aliskiren at 0.05 mg/day. Aliskiren had no effects in rats on regular salt. Neither high salt nor aliskiren affected hypothalamic ANG II content. These results indicate that intracerebroventricular infusions of aliskiren and an AT1 receptor blocker are similarly effective in preventing salt-induced sympathetic hyperactivity and hypertension in Dahl S rats, suggesting that renin in the brain plays an essential role in the salt-induced hypertension. The absence of an obvious increase in hypothalamic ANG II by high salt, or decrease in ANG II by aliskiren, suggests that tissue levels do not reflect renin-dependent ANG II production in sympathoexcitatory angiotensinergic neurons.

APA, Harvard, Vancouver, ISO, and other styles

38

Campbell, James A., Claudia J. Schröder-Adams, James W. Haggart, Patrick S. Drucken-Miller, Michael J. Ryan, and Grant D. Zazula. "First records of a Plesiosaurian (Reptilia: Sauropterygia) and an Ichthyosaur (Reptilia: Ichthyosauria) from Yukon, Canada." Canadian Field-Naturalist 127, no. 3 (December 3, 2013): 234. http://dx.doi.org/10.22621/cfn.v127i3.1489.

Full text

Abstract:

An isolated centrum collected ex situ from marine shales of the Lower Cretaceous (Albian) Arctic Red Formation along the Road River represents the first documented occurrence of a plesiosaurian from Yukon. This centrum represents the northernmost occurrence of plesiosaurians in the Western Interior Sea of North America prior to the establishment of the first continuous seaway (Western Interior Seaway) connecting the Boreal and Tethyan seas. Additionally, this centrum is potentially the second-oldest elasmosaurid specimen known from North America. A second centrum, collected along the Beaver River, is likely derived from the Lower Cretaceous (Lower Albian) Garbutt Formation exposed farther upstream. It represents the first report of an ichthyosaur from Yukon. Additionally, six associated ribs collected from the Arctic Red Formation along the Peel River may also belong to a marine reptile; however, poor preservation of these ribs prevents a definitive taxonomic assignment.

APA, Harvard, Vancouver, ISO, and other styles

39

Wright, DG. "A role for guanine ribonucleotides in the regulation of myeloid cell maturation." Blood 69, no. 1 (January 1, 1987): 334–37. http://dx.doi.org/10.1182/blood.v69.1.334.334.

Full text

Abstract:

Abstract We have shown previously that induced maturation of the human myeloid leukemia cell line, HL-60, is associated with a selective down- regulation of guanine ribonucleotide synthesis and depletion of intracellular guanosine triphosphate (GTP) and guanosine diphosphate (GDP) pools. We showed, furthermore, that inhibitors of the enzyme, inosine monophosphate (IMP) dehydrogenase, which catalyzes the initial rate-limiting step of guanylate synthesis from the central intermediate IMP, are potent inducers of myeloid maturation in these cells. We now show that induced maturation of HL-60 cells is prevented or impaired if intracellular concentrations of guanine ribonucleotides are maintained at high levels. HL-60 cells can utilize exogenous guanine and guanosine to maintain GTP and GDP pools through a salvage pathway that bypasses guanylate synthesis from IMP. Moreover, incubation of HL-60 cells with guanosine or guanine (10(-6) to 10(-4) mol/L) prevents both the depletion of intracellular guanine ribonucleotides and the induction of myeloid maturation caused by the IMP dehydrogenase inhibitor, tiazofurin. These findings provide strong additional support for the concept that terminal myeloid differentiation is influenced by a guanine ribonucleotide-dependent regulatory system.

APA, Harvard, Vancouver, ISO, and other styles

40

Wright, DG. "A role for guanine ribonucleotides in the regulation of myeloid cell maturation." Blood 69, no. 1 (January 1, 1987): 334–37. http://dx.doi.org/10.1182/blood.v69.1.334.bloodjournal691334.

Full text

Abstract:

We have shown previously that induced maturation of the human myeloid leukemia cell line, HL-60, is associated with a selective down- regulation of guanine ribonucleotide synthesis and depletion of intracellular guanosine triphosphate (GTP) and guanosine diphosphate (GDP) pools. We showed, furthermore, that inhibitors of the enzyme, inosine monophosphate (IMP) dehydrogenase, which catalyzes the initial rate-limiting step of guanylate synthesis from the central intermediate IMP, are potent inducers of myeloid maturation in these cells. We now show that induced maturation of HL-60 cells is prevented or impaired if intracellular concentrations of guanine ribonucleotides are maintained at high levels. HL-60 cells can utilize exogenous guanine and guanosine to maintain GTP and GDP pools through a salvage pathway that bypasses guanylate synthesis from IMP. Moreover, incubation of HL-60 cells with guanosine or guanine (10(-6) to 10(-4) mol/L) prevents both the depletion of intracellular guanine ribonucleotides and the induction of myeloid maturation caused by the IMP dehydrogenase inhibitor, tiazofurin. These findings provide strong additional support for the concept that terminal myeloid differentiation is influenced by a guanine ribonucleotide-dependent regulatory system.

APA, Harvard, Vancouver, ISO, and other styles

41

Lam, Carol K. L., Madhu Chari, Penny Y. T. Wang, and Tony K. T. Lam. "Central lactate metabolism regulates food intake." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E491—E496. http://dx.doi.org/10.1152/ajpendo.90481.2008.

Full text

Abstract:

The central nervous system regulates food intake (FI) and body weight (BW), but the associated mechanisms remain to be elucidated. Here we report that central injections of lactate reduced FI and BW in rodents. Inhibition of central lactate metabolism to pyruvate with the lactate dehydrogenase inhibitor oxamate abolished the central effects of lactate on FI and BW. Conversely, central injections of pyruvate recapitulated the effects of lactate. Finally, inhibition of central lactate metabolism prevented the ability of circulating lactate to lower FI and BW. Together, the data indicate that activation of central lactate metabolism lowers FI and BW.

APA, Harvard, Vancouver, ISO, and other styles

42

McLennan, Alec G., Alexey Y. Ganin, Yasuhiro Takabayashi, Ross H. Colman, Ruth H. Zadik, Matthew J. Rosseinsky, and Kosmas Prassides. "Synthesis of face-centred cubic Cs3C60 in THF." Faraday Discuss. 173 (2014): 95–103. http://dx.doi.org/10.1039/c4fd00085d.

Full text

Abstract:

A solution chemistry synthetic route yields Cs₃C₆₀ with a face-centred cubic structure. The described method uses well-established Schlenk techniques and THF as a solvent. The controlled addition of an organo-metallic salt reducing agent prevents the formation of C₆₀⁴⁻ salts. The final product can be precipitated from the solution using hexane as an anti-solvent.

APA, Harvard, Vancouver, ISO, and other styles

43

Gomez-Sanchez, E. P., and C. E. Gomez-Sanchez. "Effect of central amiloride infusion on mineralocorticoid hypertension." American Journal of Physiology-Endocrinology and Metabolism 267, no. 5 (November 1, 1994): E754—E758. http://dx.doi.org/10.1152/ajpendo.1994.267.5.e754.

Full text

Abstract:

There is strong evidence from different types of studies, including the discrete infusion of agonists and antagonists and ablation of specific brain areas or transmitter-type neurons, that mineralocorticoids, in excess, act in the brain to elevate blood pressure. Aldosterone enhances the entry of Na+ through amiloride-sensitive Na+ channels in some mineralocorticoid-sensitive transport epithelial cells. To define possible cellular mechanisms involved in central mineralocorticoid action, benzamil, an amiloride analogue with selective affinity for the Na+ channel, was continuously infused intracerebroventricularly in three mineralocorticoid-dependent hypertension models in Sprague-Dawley rats, the continuous subcutaneous infusion of aldosterone, the intracerebroventricular infusion of aldosterone, and the ingestion of carbenoxolone, a synthetic licorice analogue. The intracerebroventricular infusion of 0.3 and 0.5 micrograms/h of benzamil, doses that did not have an adverse effect on growth and that had no effect on the blood pressure when infused subcutaneously, prevented the increase in blood pressure in these models. The infusion of these levels of benzamil had no effect on urine volume even in those animals in which it prevented an increase in blood pressure. These data suggest that the central effects of mineralocorticoids on blood pressure are mediated, at least in part, by the effects of mineralocorticoids on amiloride-sensitive sodium transport.

APA, Harvard, Vancouver, ISO, and other styles

44

Milutinović, Sanja, David Murphy, and Nina Japundžić-Žigon. "The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 6 (December 2006): R1579—R1591. http://dx.doi.org/10.1152/ajpregu.00764.2005.

Full text

Abstract:

Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V1a, V1b, and V2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and high-frequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb) was also investigated. Under basal conditions, V1a antagonist increased HF-BP and Tb, and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb, and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes, whereas V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V1a and V1b but not V2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b, and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1a or V1b, but not V2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively.

APA, Harvard, Vancouver, ISO, and other styles

45

Benazzo, Andrea, Emiliano Trucchi, James A. Cahill, Pierpaolo Maisano Delser, Stefano Mona, Matteo Fumagalli, Lynsey Bunnefeld, et al. "Survival and divergence in a small group: The extraordinary genomic history of the endangered Apennine brown bear stragglers." Proceedings of the National Academy of Sciences 114, no. 45 (October 24, 2017): E9589—E9597. http://dx.doi.org/10.1073/pnas.1707279114.

Full text

Abstract:

About 100 km east of Rome, in the central Apennine Mountains, a critically endangered population of ∼50 brown bears live in complete isolation. Mating outside this population is prevented by several 100 km of bear-free territories. We exploited this natural experiment to better understand the gene and genomic consequences of surviving at extremely small population size. We found that brown bear populations in Europe lost connectivity since Neolithic times, when farming communities expanded and forest burning was used for land clearance. In central Italy, this resulted in a 40-fold population decline. The overall genomic impact of this decline included the complete loss of variation in the mitochondrial genome and along long stretches of the nuclear genome. Several private and deleterious amino acid changes were fixed by random drift; predicted effects include energy deficit, muscle weakness, anomalies in cranial and skeletal development, and reduced aggressiveness. Despite this extreme loss of diversity, Apennine bear genomes show nonrandom peaks of high variation, possibly maintained by balancing selection, at genomic regions significantly enriched for genes associated with immune and olfactory systems. Challenging the paradigm of increased extinction risk in small populations, we suggest that random fixation of deleterious alleles (i) can be an important driver of divergence in isolation, (ii) can be tolerated when balancing selection prevents random loss of variation at important genes, and (iii) is followed by or results directly in favorable behavioral changes.

APA, Harvard, Vancouver, ISO, and other styles

46

Pedley, K. C., G. E. Jones, M. Magnani, R. J. Rist, and R. J. Naftalin. "Direct observation of hexokinase translocation in stimulated macrophages." Biochemical Journal 291, no. 2 (April 15, 1993): 515–22. http://dx.doi.org/10.1042/bj2910515.

Full text

Abstract:

1. Fluorescence imaging of antibodies was used to show that phorbol 12-myristate 13-acetate (PMA) induces a 4-fold increase in the amount of hexokinase relative to the control in the cortical shell of rat peritoneal macrophage cytosol adjacent to the plasma membrane, and a corresponding depletion in the amount of hexokinase in the central core of the cytosol. However, there was no significant PMA-dependent change in the distribution of glucose-6-phosphate dehydrogenase. 2. Cytochalasin D, an inhibitor of actin microfilament polymerization, prevented the PMA-induced hexokinase translocation and also reduced the PMA-dependent increases in 2-deoxy-D-glucose transport and glucose-dependent PMA-stimulated superoxide production. 3. PMA caused a contraction of the width of the cortical F-actin zone. Cytochalasin D caused some dispersal of F-actin within the cell, increasing the density of F-actin within the central cytosolic core and causing aggregation of the F-actin within the cortex. These data are consistent with the view that PMA induces attachment of hexokinase to microfilaments within the cortical zone adjacent to the cell membrane of macrophages, and cytochalasin D prevents this attachment. This is the first direct demonstration of the translocation of hexokinase to the plasma membrane in activated cells, and supports the view that enhanced hexokinase activity in the cortical region of the cytosol is an important early component of the macrophage activation process.

APA, Harvard, Vancouver, ISO, and other styles

47

Williams, Tamara L., T. Andrew Bowdle, Bradford D. Winters, Stephen D. Pavkovic, and Marilyn K. Szekendi. "Guidewires Unintentionally Retained During Central Venous Catheterization." Journal of the Association for Vascular Access 19, no. 1 (March 1, 2014): 29–34. http://dx.doi.org/10.1016/j.java.2013.12.001.

Full text

Abstract:

Abstract Background: A number of mechanical complications can occur during the insertion of a central venous catheter (CVC), including breakage or loss of the wire and unrecognized failure to remove the wire. Complications related to retention of a guidewire can be serious or fatal. Methods: Incident reports on retained CVC guidewires entered into the University HealthSystem Consortium (UHC) Safety Intelligence Patient Safety Organization (PSO) database (Chicago, IL) over a 5-year period were reviewed to improve our understanding of their circumstances, causes, and related patient outcomes. Findings: A total of 42 events that involved retention of a whole guidewire or a fragment of a wire were found in the UHC Safety Intelligence PSO database from 2008 through 2012. Although one-third of these events were discovered during or at the end of the CVC insertion procedure, retained CVC guidewires were commonly discovered days to years after the procedure and on imaging tests performed for unrelated reasons or during other subsequent care. Managers who reviewed the events commonly recommended education and training to prevent retained CVC guidewires, but factors contributing to these events such as distractions and emergency situations also suggest the need for a device design that prevents the occurrence. Conclusions: Efforts to prevent the loss of CVC guidewires should include clinician education and the development of a device design that prevents inadvertent guidewire loss and alerts clinicians when the end of the guidewire is near.

APA, Harvard, Vancouver, ISO, and other styles

48

Zhang, Y., JT Wilsey, CD Frase, MM Matheny, BS Bender, S. Zolotukhin, and PJ Scarpace. "Peripheral but not central leptin prevents the immunosuppression associated with hypoleptinemia in rats." Journal of Endocrinology 174, no. 3 (September 1, 2002): 455–61. http://dx.doi.org/10.1677/joe.0.1740455.

Full text

Abstract:

Leptin is a peripheral immunoenhancing reagent that directly activates splenic lymphocytes in mice. We found that a 48 h fast in rats resulted in a decrease in serum leptin that was accompanied by a lower delayed-type hypersensitivity (DTH) response. Peripheral leptin replacement completely restored this response in fasted animals. We employed a recombinant adeno-associated virus (rAAV) system to deliver leptin gene directly into rat brain to assess the effect of sustained long-term central expression of leptin on immune responses. The rAAV-leptin rats had elevated central leptin over the 60 day duration of the experiment, whereas body fat and circulating leptin fell to near zero levels. The DTH response was significantly reduced by 10-20% in rats receiving rAAV-leptin compared with the control rats, and the difference was maintained for over 50 h. When the rats undergoing rAAV-leptin gene therapy were given either murine recombinant leptin or PBS s.c., rats receiving leptin had a 17% higher DTH response than rats receiving PBS. The isolated splenocytes from the former group also proliferated 34% more in vitro in response to the mitogen concanavalin A as compared with the latter group. These results suggest that peripheral leptin has a dominant role in maintaining T-cell-mediated immune responses in rats, and central leptin is unable to compensate for the immunosuppression associated with peripheral hypoleptinemia. Furthermore, preservation of normal cell-mediated immune responses does not require fat tissue as along as serum leptin levels are maintained.

APA, Harvard, Vancouver, ISO, and other styles

49

Clatterbuck, R. E., D. L. Price, and V. E. Koliatsos. "Ciliary neurotrophic factor prevents retrograde neuronal death in the adult central nervous system." Proceedings of the National Academy of Sciences 90, no. 6 (March 15, 1993): 2222–26. http://dx.doi.org/10.1073/pnas.90.6.2222.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Sluka, Kathleen A., James M. O'Donnell, Jessica Danielson, and Lynn A. Rasmussen. "Regular physical activity prevents development of chronic pain and activation of central neurons." Journal of Applied Physiology 114, no. 6 (March 15, 2013): 725–33. http://dx.doi.org/10.1152/japplphysiol.01317.2012.

Full text

Abstract:

Chronic musculoskeletal pain is a significant health problem and is associated with increases in pain during acute physical activity. Regular physical activity is protective against many chronic diseases; however, it is unknown if it plays a role in development of chronic pain. The current study induced physical activity by placing running wheels in home cages of mice for 5 days or 8 wk and compared these to sedentary mice without running wheels in their home cages. Chronic muscle pain was induced by repeated intramuscular injection of pH 4.0 saline, exercise-enhanced pain was induced by combining a 2-h fatiguing exercise task with a low-dose muscle inflammation (0.03% carrageenan), and acute muscle inflammation was induced by 3% carrageenan. We tested the responses of the paw (response frequency) and muscle (withdrawal threshold) to nociceptive stimuli. Because the rostral ventromedial medulla (RVM) is involved in exercise-induced analgesia and chronic muscle pain, we tested for changes in phosphorylation of the NR1 subunit of the N-methyl-d-aspartate (NMDA) receptor in the RVM. We demonstrate that regular physical activity prevents the development of chronic muscle pain and exercise-induced muscle pain by reducing phosphorylation of the NR1 subunit of the NMDA receptor in the central nervous system. However, regular physical activity has no effect on development of acute pain. Thus physical inactivity is a risk factor for development of chronic pain and may set the nervous system to respond in an exaggerated way to low-intensity muscle insults.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Centrum prevence'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles