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1
Krebs, Jakob, and Sabine Reh. "Freie Lerninhalte im Internet mit Studierenden recherchieren, kommentieren und kompilieren. Zur Gestaltung der online-Selbstlernangebote im hr-Funkkolleg Philosophie." Tagungsband: Bildung gemeinsam verändern: Diskussionsbeiträge und Impulse aus Forschung und Praxis 28, Bildung gemeinsam verändern (2017): 85–92. http://dx.doi.org/10.21240/mpaed/28/2017.03.01.x.
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Wie lassen sich online frei verfügbare Bildungsinhalte mit Studierenden so zusammenstellen, dass sie als thematisch sortierte Selbstlernmaterialien unkompliziert gefunden werden können – sei es von anderen Studierenden, interessierten Laien oder auch von Lehrkräften in Bildungsinstitutionen? Der vorliegende Werkstattbericht rekonstruiert ein Lernszenario, in dem Studierende vorhandene Materialien im Internet recherchierten, kommentierten und kompilierten, um ein Online-Zusatzangebot zu den Radiosendungen im hr-Funkkolleg Philosophie 2014/15 zu erstellen. Die Rahmenbedingungen dieser ungewöhnlichen universitären Kooperation mit dem Rundfunk werden im ersten Abschnitt vorgestellt. Der zweite Abschnitt skizziert das didaktische Design zusammen mit dem Projektstrukturplan eines produktorientierten kollaborativen Lernsettings mit Wiki-Einsatz. Im dritten Abschnitt werden der Lernerfolg bei den Studierenden sowie einige Herausforderungen benannt, die u. a. in der Abschlussevaluierung zur Sprache kamen. Der vierte Abschnitt macht die Projekterfahrungen für reguläre Lehr- und Lern-Szenarien fruchtbar, in denen nicht nur Studierende mit didaktischen Interessen durch die gemeinsame Gestaltung von Internetangeboten fachlich und methodisch profitieren können. Mit dem Bericht wird somit u. a. veranschaulicht, wie sich Ansätze von Blended, Peer-Assisted und Service Learning produktiv kombinieren lassen.
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Picard, Marc. "On the Effects of Frequency-Induced Phonological Change." Diachronica 14, no. 1 (1997): 109–18. http://dx.doi.org/10.1075/dia.14.1.05pic.
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SUMMARY It has long been recognized that there are two basic types of sound change: phonetic change, which is intrinsically regular, and analogical change, which is basically irregular. In addition, it has been argued by Witold Manczak that in any language, about one third of the words manifest an irregular sound change due to frequency. Such changes have in common the fact that in language after language they apply to the same lexical categories, amputating segments from forms whose length and frequency are in discordance. Although Manczak has studied this phenomenon extensively from a diachronic perspective, no one has yet looked specifically at the synchronic consequences of this type of change. What such a study reveals, inter alia, is how it is possible for an irregular sound change due to frequency to yield a regular synchronic morphophonemic rule, and also how such a morphophonemic process can emerge without first going through a strictly phonological stage. RÉSUMÉ On reconnaît depuis longtemps qu'il y a deux types de changements phonologiques: le changement phonétique, qui est intrinsèquement régulier, et le changement analogique, qui est fondamentalement irrégulier. Or voilà plusieurs années que Witold Mariczak tente de démontrer que dans toute langue, environ le tiers des mots manifeste un changement irrégulier dû à la fréquence. De tels changements ont en commun le fait que dans langue après langue, ils s'appliquent aux mêmes catégories lexicales en amputant des segments aux formes dont la longueur et la fréquence sont en déséquilibre. Bien que Mariczak ait étudié ce phénomène à fond dans une optique historique, personne n'a encore examiné de façon spécifique les conséquences synchroniques de ce type de changement. Une telle étude démontre, entre autre, qu'il est possible pour un changement phonologique irrégulier dû à la fréquence d'aboutir à une règle morphophonémique synchronique régulière, et aussi comment un tel processus morphophonémique peut surgir sans avoir passé au préalable par une étape strictement phonologique. ZUSAMMENFASSUNG Das Vorhandensein von zwei Grundtypen der Lautveränderung ist seit langem anerkannt: phonetischer Wandel, der gewöhnlich regulär ist, und aria-logischer Wandel, der als irregular gilt. Hierzu kame noch die Tatsache, laut Witold Manczak, daB in jeder Sprache etwa ein Drittel der Wörter häufig-keitsbedingten unregelmaßigen Lautwandel unterliege. Solche Veränderun-gen haben die Eigenschaft gemein, daB in einer Sprache nach der anderen stets die gleichen lexikalischen Kategorien betroffen sind, in dem sie Segmente abtrennen, deren Lange und Gebrauchshäufigkeit im Widerspruch stehen. Abschon Manczak dieses Phanomen intensiv aus der diachronischen Perspektive studiert hat, hat bis heute niemand sein Augenmerk auf die synchronen Konsequenzen dieses Veranderungstyps gerichtet. Was namlich eine solche Untersuchung zutage fördert, ist u.a. wie es möglich ist für einen irregulären Lautwandel, der durch Verwendungshäufigkeit hervorgerufen wurde, eine reguläre synchronische morphophonemische Regel hervorzu-bringen, und auch wie solch ein morphophonemischer Prozeß entstehen kann, ohne zunachst ein strikt phonologisches Stadium durchlaufen zu haben.
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Zehnder, Adalbert. "Vivantes-Managerin wird reguläre Geschäftsführerin." kma - Klinik Management aktuell 17, no. 01 (2012): 14. http://dx.doi.org/10.1055/s-0036-1576296.
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Von „zeitlich befristeter Nachbarschaftshilfe“ sprach Joachim Bovelet, als der von ihm geführte Vivantes-Verbund im August 2011 die Interimsgeschäftsführung beim finanziell angeschlagenen Klinikum Offenbach übernahm. Die Aufgabe war klar umrissen: Der selbst schwarze Zahlen schreibende kommunale Konzern aus Berlin sollte für das mit 240 Millionen Euro Schulden belastete und von Insolvenz bedrohte Haus krisenerprobtes Führungspersonal bereitstellen, den Betrieb einer Analyse unterziehen und anschließend ein Sanierungsprogramm vorlegen. Damit das Klinikum kommunal bleiben könnte, sollte zugleich während dieser Übergangszeit ein Käufer oder Partner gesucht werden. Einen Einstieg von Vivantes, über den spekuliert wurde, dementierte Bovelet stets vehement. Die Kooperation sei nicht mehr und nicht weniger als eine Solidaritätsgeste nach dem Motto „Kommunal hilft Kommunal“, nach einem halben Jahr sei Schluss.
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Kauer, Marianne, and Claudia M. Roebers. "Kognitive Basisfunktionen und motorisch-koordinative Kompetenzen in Abhängigkeit des Peerstatus bei Kindern zu Beginn der Schulzeit." Zeitschrift für Entwicklungspsychologie und Pädagogische Psychologie 44, no. 3 (2012): 139–52. http://dx.doi.org/10.1026/0049-8637/a000065.
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Zusammenfassung. In der vorliegenden Studie wird der Frage nachgegangen, ob sich zwischen beliebten, durchschnittlichen, unbeachteten und zurückgewiesenen Kindern Unterschiede in spezifischen kognitiven und motorischen Fähigkeiten finden lassen. Zu drei verschiedenen Zeitpunkten wurden mit 177 regulär eingeschulten 7-jährigen Kindern Peernominationen und Peerratings erhoben, um reliable soziometrische Daten zu erhalten und ein Vergleich der beiden Methoden vorzunehmen. Außerdem wurde eine umfassende Testbatterie von insgesamt 20 Aufgaben in den Bereichen Informationsverarbeitungsgeschwindigkeit, Kurzzeit- und Arbeitsgedächtnis, Inhibition, Sprache und Motorik durchgeführt. Mit Ausnahme der Kurzzeitgedächtniskapazität wurden für alle Funktionsbereiche signifikante Unterschiede zwischen den Statusgruppen gefunden. Die kontinuierlichen soziometrischen Werte der Ratingmethode zeigten sich etwas sensitiver als die der Nominationsmethode. Korrelativ wurde mit beiden Methoden ersichtlich, dass bessere Leistungen im kognitiven und motorischen Bereich nicht nur mit mehr Beliebtheit zusammenhingen, sondern auch, dass schlechte Leistungen in Verbindung standen mit sozialer Zurückweisung.
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Norman, M. Ursula, Rebecca A. Lew, A. Ian Smith, and Michael J. Hickey. "Metalloendopeptidases EC 3.4.24.15/16 regulate bradykinin activity in the cerebral microvasculature." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (2003): H1942—H1948. http://dx.doi.org/10.1152/ajpheart.00948.2002.
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Bradykinin is a vasoactive peptide that has been shown to increase the permeability of the cerebral microvasculature to blood-borne macromolecules. The two zinc metalloendopeptidases EC 3.4.24.15 (EP 24.15) and EC 3.4.24.16 (EP 24.16) degrade bradykinin in vitro and are highly expressed in the brain. However, the role that these enzymes play in bradykinin metabolism in vivo remains unclear. In the present study, we investigated the role of EP 24.15 and EP 24.16 in the regulation of bradykinin-induced alterations in microvascular permeability. Permeability of the cerebral microvasculature was assessed in anesthetized Sprague-Dawley rats by measuring the clearance of 70-kDa FITC dextran from the brain. Inhibition of EP 24.15 and EP 24.16 by the specific inhibitor N-[1-( R, S)-carboxy-3-phenylpropyl]-Ala-Aib-Tyr- p-aminobenzoate (JA-2) resulted in the potentiation of bradykinin-induced increases in cerebral microvessel permeability. The level of potentiation was comparable to that achieved by the inhibition of angiotensin-converting enzyme. These findings provide the first evidence of an in vivo role for EP 24.15/EP 24.16 in brain function, specifically in regulating alterations in microvessel permeability induced by exogenous bradykinin.
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Sasso, Corina Verónica, Flavia Eliana Santiano, Fiorella Campo Verde Arboccó, et al. "Estradiol and progesterone regulate proliferation and apoptosis in colon cancer." Endocrine Connections 8, no. 3 (2019): 217–29. http://dx.doi.org/10.1530/ec-18-0374.
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Epidemiological studies describe estrogens as protectors in the development of colon cancer in postmenopausal women treated with hormone replacement therapy. However, the role of progesterone in colon cancer has been minimally studied and the results are controversial. For the above, the objective of this work was to determine the hormonal regulation exerted by natural ovarian steroids on proliferation and apoptosis in an experimental model of colon cancer in ovariectomized rats treated with 17-beta estradiol and progesterone. Sprague–Dawley rats were exposed to the carcinogen 1,2-dimethylhydrazine to induce colon tumors. Thirty days later, the rats were ovariectomized and treated with estradiol (60 μg/kg), progesterone (10 mg/kg), estradiol plus progesterone (60 μg/kg and 10 mg/kg) or vehicle. We observed no significant differences in colon cancer incidence and tumor multiplicity between the groups. Nevertheless, we observed a decrease in PCNA expression and a greater number of apoptotic index, higher expression of caspase 3, cleaved PARP and cleaved caspase 8 in tumors, confirming the activation of the extrinsic pathway of apoptosis by the combined treatment. In addition, we observed a higher expression of estrogen receptor beta in these tumors. We conclude that the action of both hormones, estradiol and progesterone, is necessary to reduce proliferation and increase apoptosis in colon tumors, probably through estrogen receptor beta activation.
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Zhang, Xiaoxia, Zumin Xing, Jiyuan Li, Shuyi Tang та Yiwen Zhang. "Gold Nanoparticles with Dexmedetomidine Regulate GSK-3β to Reduce Neurocognitive Effects in Anesthetized Rats". Journal of Nanoscience and Nanotechnology 21, № 12 (2021): 6205–11. http://dx.doi.org/10.1166/jnn.2021.18745.
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The aim of this study was to explore the neurocognitive effects of dexmedetomidine-loaded gold nanoparticles (AuNPs-dexmedetomidine) on anesthetized rats. Sixty Sprague Dawley rats (age, 2–3 weeks; weight, 250–280 g) were randomly divided into three groups (n = 20): the control group and two groups that received intraperitoneal injection of AuNPs-dexmedetomidine at 50 and 100 μg/kg each. Western blotting and RT-PCR were used to determine the protein and mRNA expression of GSK-3β, respectively. Compared with that in the control group, GSK-3β expression in AuNP-dexmedetomidine groups increased (P < 0.05). The protein expression of GSK-3β was higher and mRNA expression was significantly lower in the 100 μg/kg AuNP-dexmedetomidine group (P < 0.05). AuNPs-dexmedetomidine reduced the neurocognitive effect on anesthetized rats through the regulation of the GSK-3β signaling pathway.
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VanLandingham, Jacob W., Milos Cekic, Sarah M. Cutler, et al. "Progesterone and its Metabolite Allopregnanolone Differentially Regulate Hemostatic Proteins after Traumatic Brain Injury." Journal of Cerebral Blood Flow & Metabolism 28, no. 11 (2008): 1786–94. http://dx.doi.org/10.1038/jcbfm.2008.73.
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Our laboratory has shown in numerous experiments that the neurosteroids progesterone (PROG) and allopregnanolone (ALLO) improve molecular and functional outcomes after traumatic brain injury (TBI). As coagulopathy is an important contributor to the secondary destruction of nervous tissue, we hypothesized that PROG and ALLO administration may also have a beneficial effect on coagulation protein expression after TBI. Adult male Sprague—Dawley rats were given bilateral contusions of the medial frontal cortex followed by treatments with PROG (16 mg/kg), ALLO (8 mg/kg), or vehicle (22.5% hydroxypropyl-β-cyclodextrin). Controls received no injury or injections. Progesterone generally maintained procoagulant (thrombin, fibrinogen, and coagulation factor XIII), whereas ALLO increased anticoagulant protein expression (tissue-type plasminogen activator, tPA). In addition, PROG significantly increased the ratio of tPA bound to neuroserpin, a serine protease inhibitor that can reduce the activity of tPA. Our findings suggest that in a model of TBI, where blood loss may exacerbate injury, it may be preferable to treat patients with PROG, whereas it might be more appropriate to use ALLO as a treatment for thrombotic stroke, where a reduction in coagulation would be more beneficial.
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Berlach, Anna Viktorivna. "Issues on the Definition of Administrative-Legal System of Principles for Regulation of Natural Monopoly Subjects’ Activities in the Sector of Electric Power Engineering in Ukraine." Przegląd Prawa Administracyjnego 2 (November 29, 2020): 11–21. http://dx.doi.org/10.17951/ppa.2019.2.11-21.
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The article deals with the analysis of modern scientific views on determining the content of the principles for legal regulation development. In particular, the author investigates issues of administrative and legal regulation of natural monopoly entities activity in the field of electric power engineering in Ukraine. Ths way of author’s approach can be explained by the peculiarities of relations in the sector of electric energy production in Ukraine. These peculiarities include: the necessity to regulate competition on electricity market, prevention of corruption and other negative consequences of the monopoly, as well as the increasing of investment attractiveness in the electric power sector. Th author shows that the relevance of this research is determined by the dynamic development of legislation within this industry along with conditions of legal relations in the field of electricity, in particular, the launch of new entities into the electricity market. There it is shown that the current legislation of Ukraine defines the relevant standards of functioning of the electricity market, concerning general approaches to the content of state policy in this sector of economy. At the same time, it was emphasized that the system of principles for administrative and legal regulation of the subjects of natural monopolies activity in the field of electricity is subject to further investigation. The content of sectoral legislation governing the electricity sector and anti-monopoly one that defines the legal status of natural monopoly entities are analyzed in detail. It is shown that at present time the authorities that are to legislate these principles have established them just in some certain areas of administrative and legal regulation in this field without proper systematic and scientifically grounded approach. According to the author’s idea, such a situation may complicate the law enforcement practice, since the question of the application of a particular system of principles remains dim. Th author has formulated the conclusion on the need for improvement of sectoral legislation, which would ensure balance of interests between manufacturers and consumers of electricity, taking into account the whole economic system of the country.
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Vitulli, William F., Mary L. Rust, Pamela M. Mortellaro, Joseph M. Quinn, Jane M. Barbin, and A. Nicholas DePace. "Alcohol Effects on Behavioral Thermoregulation with Microwave Radiation." Psychological Reports 70, no. 3_suppl (1992): 1160–62. http://dx.doi.org/10.2466/pr0.1992.70.3c.1160.
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Ethanol may play an active role in modifying “set point” levels in conjunction with behavioral thermoregulation. A geometric series of doses of ethanol solutions was administered (ip) prior to fixed-interval 2-min. schedules of microwave reinforcement in rats tested in a cold environment. Four Sprague-Dawley rats were conditioned to regulate their thermal environment with 5-sec. exposures of MW reinforcement. Friedman's nonparametric test showed significant differences between ethanol doses, and Sign tests showed that moderate and high doses of ethanol suppressed operant behavior reinforced by MW radiation. Interactions between changes in “set-point” and discriminative properties of ethanol are discussed.
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Rodrigues, Brian, and David L. Severson. "Acute diabetes does not reduce heparin-releasable lipoprotein lipase activity in perfused hearts from Wistar–Kyoto rats." Canadian Journal of Physiology and Pharmacology 71, no. 9 (1993): 657–61. http://dx.doi.org/10.1139/y93-096.
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The induction of diabetes (3–5 days duration) in Wistar–Kyoto rats by the administration of streptozotocin (100 mg/kg) did not increase plasma concentrations of triacylglycerols or free fatty acids, and did not reduce heparin-releasable (functional) lipoprotein lipase activity in perfused hearts. By comparison, diabetic Sprague–Dawley rats were characterized as having hypertriglyceridemia and decreased heparin-releasable lipoprotein lipase activity in perfused hearts. Therefore, the diabetes-induced reduction in myocardial lipoprotein lipase activity in Sprague–Dawley rat hearts may, at least in part, be a compensatory response to the hypertriglyceridemia and increased fatty acid delivery to the myocardial cell, which is a characteristic feature of most severe, insulin-deficient models of diabetes mellitus. Although functional, endothelium-bound lipoprotein lipase activity was not reduced in diabetic perfused hearts from Wistar–Kyoto rats, cellular and heparin-releasable lipoprotein lipase activity was reduced in cardiac myocyte preparations, suggesting that other mechanisms in addition to plasma triacylglycerol must regulate lipoprotein lipase activity in the whole diabetic Wistar–Kyoto rat heart and that cardiac myocytes may not be the exclusive source of functional lipoprotein lipase in the diabetic myocardium.Key words: diabetes, hypertriglyceridemia, lipoprotein lipase, perfused hearts, cardiac myocytes.
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Cao, Jieyun, Michael Ng, and Melanie A. Felmlee. "Sex Hormones Regulate Rat Hepatic Monocarboxylate Transporter Expression and Membrane Trafficking." Journal of Pharmacy & Pharmaceutical Sciences 20, no. 1 (2017): 435. http://dx.doi.org/10.18433/j3ch29.
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Purpose: Monocarboxylate transporters (MCTs) are involved in the transport of monocarboxylates such as ketone bodies, lactate, and pharmaceutical agents. CD147 functions as an ancillary protein for MCT1 and MCT4 for plasma membrane trafficking. Sex differences in MCT1 and MCT4 have been observed in muscle and reproductive tissues; however, there is a paucity of information on MCT sex differences in tissues involved in drug disposition. The objective of the present study was to quantify hepatic MCT1, MCT4 and CD147 mRNA, total cellular and membrane protein expression in males, over the estrous cycle in females and in ovariectomized (OVX) females. Method: Liver samples were collected from females at the four estrous cycle stages (proestrus, estrus, metestrus, diestrus), OVX females and male Sprague-Dawley rats (N = 3 – 5). Estrus cycle stage of females was determined by vaginal lavage. mRNA and protein (total and membrane) expression of MCT1, MCT4 and CD147 was evaluated by qPCR and western blot analysis. Results: MCT1 mRNA and membrane protein expression varied with estrous cycle stage, with OVX females having higher expression than males, indicating that female sex hormones may play a role in MCT1 regulation. MCT4 membrane expression varied with estrous cycle stage with expression significantly lower than males. MCT4 membrane expression in OVX females was also lower than males, suggesting that androgens play a role in membrane expression of MCT4. Males had higher membrane CD147 expression, whereas there was no difference in whole cell protein and mRNA levels suggesting that androgens are involved in regulating CD147 membrane localization. Conclusions: This study demonstrates hepatic expression and membrane localization of MCT1, MCT4 and CD147 are regulated by sex hormones. Sex differences in hepatic MCT expression may lead to altered drug disposition, so it is critical to elucidate the underlying mechanisms in the sex hormone-dependent regulation of MCT expression. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.
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Appel, R. G., J. Wang, M. S. Simonson, and M. J. Dunn. "A mechanism by which atrial natriuretic factor mediates its glomerular actions." American Journal of Physiology-Renal Physiology 251, no. 6 (1986): F1036—F1042. http://dx.doi.org/10.1152/ajprenal.1986.251.6.f1036.
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Differential in vivo glomerular effects of atriopeptin I (AP I) and atriopeptin III (AP III) were studied in parallel with in vitro physiological and biochemical parameters. In anesthetized Sprague-Dawley rats, AP III, but not AP I, significantly increased glomerular filtration rate. Image analysis microscopy was used to assess the effect of AP I and AP III on angiotensin II (ANG II)-induced contraction of cultured rat glomerular mesangial cells. AP III, but not AP I, inhibited ANG II-induced mesangial cell contraction in a concentration-dependent manner. Additional inhibitory agents included exogenous DBcGMP, 8-BrcGMP, Na nitroprusside, and DBcAMP. AP III stimulated mesangial cell cGMP with a lower threshold and greater maximum stimulation than AP I. Neither agent stimulated cAMP accumulation. Since mesangial cell contractility may regulate the glomerular capillary surface area, these results suggest that AP III partially mediates its glomerular effects through inhibition of ANG II-induced mesangial cell contraction. Whereas cGMP is not clearly implicated as the mediator of this effect, it appears that both cGMP and cAMP may regulate the state of mesangial cell contractility.
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Nogueiras, Ruben, Sulay Tovar, Sharon E. Mitchell, et al. "Negative energy balance and leptin regulate neuromedin-U expression in the rat pars tuberalis." Journal of Endocrinology 190, no. 2 (2006): 545–53. http://dx.doi.org/10.1677/joe.1.06577.
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Central neuromedin U (NMU) functions in energy balance, the hypothalamic–pituitary–adrenal axis, LH release and circadian rhythmicity. In rats, high levels of NMU occur in the hypothalamic suprachiasmatic nuclei and the pars tuberalis of the pituitary. NMU expression in the pars tuberalis appears to be downregulated in the Zucker fatty (fa/fa) rat, lacking functional leptin receptors. In contrast, in the dorsomedial (DMH) nuclei of the mouse, NMU expression is higher in the ob/ob mouse, lacking leptin, and is upregulated by fasting. However, leptin appears not to change NMU gene expression in either the mouse DMH or the rat pars tuberalis. Thus, the present study aims to better identify factors influencing central NMU expression in the rat pars tuberalis. Sprague–Dawley rats were fasted and/or challenged with intracerebroventricular leptin or ghrelin and gene expression was measured using real-time reverse transcriptase-PCR and quantitative in situ hybridisation with riboprobes specific for NMU and NMU receptor (NMU-R2). NMU expression in the rat pars tuberalis was elevated by fasting. Ghrelin administration had no effect on the level of NMU expression, but leptin was found to diminish the expression in a concentration- and time-dependent manner. NMU-R2 expression was unchanged in any of the groups measured. These results suggest that NMU expression in rat pars tuberalis is upregulated in states of negative energy balance, and this may be mediated indirectly by changes in leptin levels. These results demonstrate a link between energy balance and NMU expression in the pars tuberalis of the pituitary.
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Beardsley, A. J., D. M. Robertson та L. O'Donnell. "127. An α6β1-integrin/focal adhesion kinase complex may regulate spermiation and spermiation failure". Reproduction, Fertility and Development 16, № 9 (2004): 127. http://dx.doi.org/10.1071/srb04abs127.
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Spermiation is the final step of spermatogenesis (sperm production) where mature spermatids are released from the somatic Sertoli cells. Spermiation is hormone sensitive; testosterone (T) and FSH withdrawal causes a disruption to the disengagement of spermatids, which are instead retained by Sertoli cells. The mechanisms involved with spermatid release and retention are not understood. We showed previously that an unknown adhesion junction containing β1-integrin persisted on retained spermatids suggesting that a defect in this adhesion complex at disengagement may underlie spermiation failure. The aim of this study is to identify the α-integrin dimerised with β1-integrin and investigate the role of phosphorylated FAK, a kinase that is involved with integrin-mediated cell adhesion, during spermiation and spermiation failure. Four adult Sprague-Dawley rats received T and oestradiol implants and FSH antibody for 7A days to suppress testicular T and FSH and induce spermiation failure. Using immunohistochemistry, α6-integrin (but not α4-integrin) and FAK-Tyr397 were localised on the Sertoli cell plasma membrane adjacent to mature spermatids. This localisation was observed until the point of spermatid release and remained on the Sertoli cell that surrounded retained spermatids after hormone suppression. A similar localisation has been previously observed with β1-integrin, suggesting that all three form a complex at the site of disengagement. To look at the function of FAK-Tyr397, comparative Western blot analysis is currently being undertaken on seminiferous tubules specific for spermiation from control and treated animals. Preliminary studies suggest that FAK-Tyr397 remains phosphorylated during spermiation failure, suggesting that FAK dephosphorylation may be important for the function of spermatid-associated adhesion complexes, as has been demonstrated in other adhesion systems. In conclusion, α6β1-integrin/FAK-containing adhesion complexes are associated with spermatids during spermiation, and the function of such complexes are likely to be perturbed during spermiation failure.
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Vitulli, William F., Rwanda Aker, Stanley W. Howard, Wendy M. Jones, Morgan W. Kimball, and Joseph M. Quinn. "Salty Solutions: Their Effects on Thermal Set Points in Behavioral Repertoires of Albino Rats." Perceptual and Motor Skills 79, no. 1 (1994): 211–15. http://dx.doi.org/10.2466/pms.1994.79.1.211.
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Salt (sodium chloride) has been linked to increased blood pressure and a rise in core body temperature. The objective of this study was to investigate the role played by salt in altering behavioral thermoregulation in albino rats. Different doses of sodium chloride were administered (ip) prior to fixed-interval 2-min. schedules of microwave reinforcement in rats tested in a cold Skinner Box. Three Sprague-Dawley rats were conditioned to regulate their thermal environment with 5-sec. exposures of MW reinforcement in a repeated-measures reversal design. Friedman's non-parametric test showed significant differences among sodium chloride doses and physiologically normal saline. Post hoc sign tests showed that all doses of NaCI suppressed operant behavior for heat except 60 mg/kg. The hypothesis that sodium chloride lowers hypothalamic set point for heat was partially supported.
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David Sandino, Juan, Dario Amaya Hurtado, and Olga Lucia Ramos. "Prediction of Reproductive System Affectation in Sprague Dawley Rats by Food Intake Exposed with Fenthion, Using Naïve Bayes Classifier and Genetic Algorithms." Biosciences, Biotechnology Research Asia 14, no. 4 (2017): 1291–97. http://dx.doi.org/10.13005/bbra/2572.
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ABSTRACT: Improper application of pesticides in agricultural crops and indirect effects caused by exposure to them through consumption of contaminated crops, nowadays represent a serious risk to public health harmony. It is vital then, to know the degree of toxicity of each of these chemicals in order to properly regulate its application and sensitize the population at risk. Therefore, this paper shows the results of an algorithm with the ability to predict the effects on the reproductive system in Sprague Dawley rats, caused by the intake of food exposed with Fenthion. The original data were processed using the Naïve Bayes classifier, then optimized using genetic algorithms. It is concluded that the prediction algorithm does the job properly, processing qualitative information with relatively low computational cost, which allows its easy portability to different development platforms.
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Gauthier, Elizabeth A., Sarah E. Guzick, Chad M. Brummett, Helen A. Baghdoyan, and Ralph Lydic. "Buprenorphine Disrupts Sleep and Decreases Adenosine Concentrations in Sleep-regulating Brain Regions of Sprague Dawley Rat." Anesthesiology 115, no. 4 (2011): 743–53. http://dx.doi.org/10.1097/aln.0b013e31822e9f85.
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Background Buprenorphine, a partial μ-opioid receptor agonist and κ-opioid receptor antagonist, is an effective analgesic. The effects of buprenorphine on sleep have not been well characterized. This study tested the hypothesis that an antinociceptive dose of buprenorphine decreases sleep and decreases adenosine concentrations in regions of the basal forebrain and pontine brainstem that regulate sleep. Methods Male Sprague Dawley rats were implanted with intravenous catheters and electrodes for recording states of wakefulness and sleep. Buprenorphine (1 mg/kg) was administered systemically via an indwelling catheter and sleep-wake states were recorded for 24 h. In additional rats, buprenorphine was delivered by microdialysis to the pontine reticular formation and substantia innominata of the basal forebrain while adenosine was simultaneously measured. Results An antinociceptive dose of buprenorphine caused a significant increase in wakefulness (25.2%) and a decrease in nonrapid eye movement sleep (-22.1%) and rapid eye movement sleep (-3.1%). Buprenorphine also increased electroencephalographic delta power during nonrapid eye movement sleep. Coadministration of the sedative-hypnotic eszopiclone diminished the buprenorphine-induced decrease in sleep. Dialysis delivery of buprenorphine significantly decreased adenosine concentrations in the pontine reticular formation (-14.6%) and substantia innominata (-36.7%). Intravenous administration of buprenorphine significantly decreased (-20%) adenosine in the substantia innominata. Conclusions Buprenorphine significantly increased time spent awake, decreased nonrapid eye movement sleep, and increased latency to sleep onset. These disruptions in sleep architecture were mitigated by coadministration of the nonbenzodiazepine sedative-hypnotic eszopiclone. The buprenorphine-induced decrease in adenosine concentrations in basal forebrain and pontine reticular formation is consistent with the interpretation that decreasing adenosine in sleep-regulating brain regions is one mechanism by which opioids disrupt sleep.
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Qin, Wen-yi, Yong Luo, Ling Chen та ін. "Electroacupuncture Could Regulate the NF-κB Signaling Pathway to Ameliorate the Inflammatory Injury in Focal Cerebral Ischemia/Reperfusion Model Rats". Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/924541.
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The activated nuclear factor-KappaB signaling pathway plays a critical role in inducing inflammatory injury. It has been reported that electroacupuncture could be an effective anti-inflammatory treatment. We aimed to explore the complex mechanism by which EA inhibits the activation of the NF-κB signal pathway and ameliorate inflammatory injury in the short term; the effects of NEMO Binding Domain peptide for this purpose were compared. Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 hrs. Total 380 male Sprague-Dawley rats are in the study. The neurobehavioral scores, infarction volumes, and the levels of IL-1βand IL-13 were detected. NF-κB p65, IκBα, IKKα, and IKKβwere analyzed and the ability of NF-κB binding DNA was investigated. The EA treatment and the NBD peptide treatment both reduced infarct size, improved neurological scores, and regulated the levels of IL-1βand IL-13. The treatment reduced the expression of IKKαand IKKβand altered the expression of NF-κB p65 and IκBαin the cytoplasm and nucleus; the activity of NF-κB was effectively reduced. We conclude that EA treatment might interfere with the process of NF-κB nuclear translocation. And it also could suppress the activity of NF-κB signaling pathway to ameliorate the inflammatory injury after focal cerebral ischemia/reperfusion.
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Hwang, E. F., I. Williams, G. Kovacs, et al. "Impaired ability of the Na+/Ca2+exchanger from the Dahl/Rapp salt-sensitive rat to regulate cytosolic calcium." American Journal of Physiology-Renal Physiology 284, no. 5 (2003): F1023—F1031. http://dx.doi.org/10.1152/ajprenal.00121.2002.
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We previously cloned Na+/Ca2+ exchanger (NCX1) from mesangial cells of salt-sensitive (SNCX = NCX1.7) and salt-resistant (RNCX = NCX1.3) Dahl/Rapp rats. The abilities of these isoforms to regulate cytosolic Ca2+ concentration ([Ca2+]i) were assessed in fura 2-loaded OK cells expressing the vector (VOK), RNCX (ROK), and SNCX (SOK). Baseline [Ca2+]i was 98 ± 20 nM ( n = 12) in VOK and was significantly lower in ROK (44 ± 5 nM; n = 12) and SOK (47 ± 13 nM; n = 12) cells. ATP at 100 μM increased [Ca2+]i by 189 ± 55 nM ( n = 12), 21 ± 9 nM ( n = 12), and 69 ± 18 nM ( n = 12) in VOK, ROK, and SOK cells, respectively. ATP (1 mM) or bradykinin (0.1 mM) caused large increases in [Ca2+]i and ROK but not SOK cells were much more efficient in reducing [Ca2+]i back to baseline levels. Parental Sprague-Dawley rat mesangial cells express both RNCX (SDRNCX) and SNCX (SDSNCX). SDRNCX and RNCX are identical at every amino acid residue, but SDSNCX and SNCX differ at amino acid 218 where it is isoleucine in SDSNCX and not phenylalanine. OK cells expressing SDSNCX (SDSOK) reduced ATP (1 mM)-induced [Ca2+]i increase back to baseline at a rate equivalent to that for ROK cells. PKC downregulation significantly attenuated the rate at which ROK and SDSOK cells reduced ATP-induced [Ca2+]i increase but had no effect in SOK cells. The reduced efficiency of SNCX to regulate [Ca2+]i is attributed, in part, to the isoleucine-to-phenylalanine mutation at amino acid 218.
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Xu, Lili, Zhe Wang, and Lixiang Deng. "Effect of Vaspin on Myocardial Ischemia-Reperfusion Injury Rats and Expression of NLR Family Pyrin Domain Containing 3 (NLRP3)." Journal of Biomaterials and Tissue Engineering 10, no. 6 (2020): 895–900. http://dx.doi.org/10.1166/jbt.2020.2342.
Full textAbstract:
Myocardial ischemia-reperfusion injury (MIRI) can cause myocardial damage. Vaspin can protect against myocardial damage. However, the effect of vaspin on MIRI rats and the expression of NLRP3 remains unclear. Sprague-Dawley rats were separated into sham group; MIRI group and Vaspin group, in which 100 ng/ml vaspin was administrated before model preparation followed by analysis of cardiac function by M-mode ultrasound, level of NLRP3, of type I collagen, IL-6 and TNF-α by ELISA, SOD activity and ROS by spectrophotometry and Bcl-2 and PI3K/AKT signaling protein expression by Western Blot. In MIRI group, left ventricular end-systolic diameter (LVESD), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), NLRP3 expression, contents of type I collagen, IL-6, TNF-α as well as ROS were significantly increased and SOD activity was significantly decreased with decreased Bcl-2 expression and upregulated pAKT and pPI3K (P < 0.05). In Vaspin group, LVESD, LVMI and LVEDD and NLRP3 expression as well as type I collagen, IL-6, TNF-α and ROS was decreased, SOD activity and Bcl-2 expression was significantly increased with downregulated pAKT and pPI3K (P < 0.05). Vaspin can regulate PI3K/AKT signaling pathway, inhibit NLRP3 expression, regulate oxidative stress, inhibit inflammation, reduce apoptosis, improve and improve cardiac function of myocardial ischemia-reperfusion injury in rats.
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Vitulli, William F., Kendra L. M. Laconsay, Andrea C. Agnew, et al. "Aspirin (Acetylsalicylic Acid) Effects on Behavioral Thermoregulation with Microwave Radiation." Perceptual and Motor Skills 77, no. 1 (1993): 187–91. http://dx.doi.org/10.2466/pms.1993.77.1.187.
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Aspirin is a widely used over-the-counter drug in our society which has wide therapeutic value, yet not all of the behavioralside effects have been studied. Different doses of aspirin solutions were administered (ip) prior to fixed-interval 2-min. schedules of microwave reinforcement in rats tested in a cold environment. Four Sprague-Dawley rats were conditioned to regulate their thermal environment with 5-sec. exposures of MW reinforcement. Friedman's nonparametric test showed significant differences among aspirin and saline-control doses. Post hoc sign tests showed that a moderate dose of aspirin increased operant behavior reinforced by MW radiation, yet lower and higher doses decreased and then increased the rate of responding which resulted in an inverted U-shaped trend. Possible multiple effects of aspirin in terms of its thermoregulatory as well as its pain-tolerance properties, and implications for hypothalamic “set point” are discussed.
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Liu, Limin, and David L. Severson. "Regulation of myocardial lipoprotein lipase activity by diabetes and thyroid hormones." Canadian Journal of Physiology and Pharmacology 72, no. 11 (1994): 1259–64. http://dx.doi.org/10.1139/y94-180.
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Administration of streptozotocin (100 mg/kg) to adult Sprague–Dawley rats reduced both functional (heparin releasable) lipoprotein lipase activity in perfused hearts and total and heparin-releasable lipoprotein lipase activity in isolated cardio-myocytes, and produced a hypothyroid state (decreased plasma levels of triiodothyronine and thyroxine). Administration of replacement doses of triiodothyronine (3 or 10 μg/kg for 3 days) to diabetic rats normalized heparin-releasable lipoprotein lipase activity in perfused hearts, but the depressed lipoprotein lipase activity in cardiomyocytes from diabetic hearts was unchanged by in vivo thyroid hormone treatment. However, hypothyroidism in thyroidectomized rats did not alter lipoprotein lipase activity in either perfused hearts or isolated cardiomyocytes. Therefore, thyroid hormones may interact with some other factor(s) in this acute, insulin-deficient model of diabetes to selectively regulate functional, heparin-releasable lipoprotein lipase activity in perfused hearts.Key words: diabetes, hypothyroidism, lipoprotein lipase, perfused hearts, cardiomyocytes.
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Chichger, Havovi, Alexander Vang, Kelly A. O'Connell та ін. "PKC δ and βII regulate angiotensin II-mediated fibrosis through p38: a mechanism of RV fibrosis in pulmonary hypertension". American Journal of Physiology-Lung Cellular and Molecular Physiology 308, № 8 (2015): L827—L836. http://dx.doi.org/10.1152/ajplung.00184.2014.
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Pulmonary hypertension (PH) eventually leads to right ventricular (RV) fibrosis and dysfunction that is associated with increased morbidity and mortality. Although angiotensin II plays an important role in RV remodeling associated with hypoxic PH, the molecular mechanisms underlying RV fibrosis in PH largely remain unresolved. We hypothesized that PKC-p38 signaling is involved in RV collagen accumulation in PH and in response to angiotensin II stimulation. Adult male Sprague-Dawley rats were exposed to 3 wk of normoxia or hypoxia (10% FiO2) as a model of PH. Hypoxic rats developed RV hypertrophy and fibrosis associated with an increase in PKC βII and δ protein expression and p38 dephosphorylation in freshly isolated RV cardiac fibroblasts. Further mechanistic studies were performed in cultured primary cardiac fibroblasts stimulated with angiotensin II, a key activator of ventricular fibrosis in PH. Angiotensin II induced a reduction in p38 phosphorylation that was attenuated following chemical inhibition of PKC βII and δ. Molecular and chemical inhibition of PKC βII and δ abrogated angiotensin II-induced cardiac fibroblast proliferation and collagen deposition in vitro. The effects of PKC inhibition on proliferation and fibrosis were reversed by chemical inhibition of p38. Conversely, constitutive activation of p38 attenuated angiotensin II-induced increase of cardiac fibroblast proliferation and collagen accumulation. PKC βII- and δ-dependent inactivation of p38 regulates cardiac fibroblast proliferation and collagen deposition in response to angiotensin II, which suggests that the PKC-p38 signaling in cardiac fibroblasts may be involved and important in the pathophysiology of RV fibrosis in PH.
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Toth, Michael J., Eric T. Poehlman, Dwight E. Matthews, André Tchernof, and Michael J. MacCoss. "Effects of estradiol and progesterone on body composition, protein synthesis, and lipoprotein lipase in rats." American Journal of Physiology-Endocrinology and Metabolism 280, no. 3 (2001): E496—E501. http://dx.doi.org/10.1152/ajpendo.2001.280.3.e496.
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Prior studies suggest that estradiol and progesterone regulate body composition in growing female rats. Because these studies did not consider the confounding effect of changes in food intake, it remains unclear whether ovarian hormones regulate body composition independently of their effects on food intake. We utilized a pair-feeding paradigm to examine the effects of these hormones on body composition. In addition, skeletal muscle protein fractional synthesis rate and adipose tissue lipoprotein lipase activity were measured to examine pathways of substrate deposition into fat and fat-free tissue. Female Sprague-Dawley rats [pubertal: 7–8 wk old; 190 ± 0.5 (SE) g] were separated into four groups: 1) sham-operated (S; n = 8), 2) ovariectomized plus placebo (OVX; n = 8), 3) ovariectomized plus estradiol (OVX+E; n = 8), and 4) ovariectomized plus progesterone (OVX+P; n = 8). All ovariectomized groups were pair-fed to the S group. Body composition was measured using total body electrical conductivity. The relative increase in fat-free mass was greater ( P < 0.01) in the OVX group (31 ± 2%) than in the S (17 ± 2%), OVX+E (18 ± 2%), and OVX+P (22 ± 2%) groups. The fractional synthetic rates of gastrocnemius muscle protein paralleled changes in fat-free mass: OVX had a higher ( P < 0.05) synthesis rate (21 ± 3%/day) than S (12 ± 2%/day), OVX+E (11 ± 2%/day), and OVX+P (8 ± 1%/day) groups. Body fat increased in the S group (31 ± 7%; P < 0.01), whereas the OVX groups lost fat (OVX: −10 ± 7%; OVX+E: −15 ± 7%; OVX+P: −13 ± 7%). No differences in lipoprotein lipase were found. Our results suggest that estradiol and progesterone may regulate the growth of fat and fat-free tissues in female rats. Moreover, ovarian hormones may influence skeletal muscle growth through their effects on skeletal muscle protein synthesis.
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Sar, T. T., U. E. Umeh, and D. Ishaleku. "Effects of B. bacteriovorus (ATCC™ 1534) Injection on Some Serum Chemistry Parameters in Rats Injected with P. multocida." NIGERIAN ANNALS OF PURE AND APPLIED SCIENCES 1 (March 13, 2019): 76–81. http://dx.doi.org/10.46912/napas.67.
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To determine effects of Bdellovibrio bacteriovorus on some serum chemistry parameters, and evaluate its ability to regulate in vivo damage and control pathogen activity, twelve Sprague Dawley rats were injected subcutaneously, once daily, with 1 x 108/ml B. bacteriovorus (ATCC™ 1534) in saline and some serumchemistry parameters measured. Another set of 12 Sprague Dawley rats were also injected once daily with 108/ml of the pathogen P. multocida. Further, 12 other rats were injected with 1 x 108/ml each of B. bacteriovorus and then with P. multocida. All injections were for 168 hours. A group of 12 rats were injected intramuscularly once, at collection of blood samples, with 2 mg/kg of Ketamine Hydrochloride, used as anaesthesia. A final group of 12 rats, not injected with any of the bacteria or anaesthetic served as controls. Blood was collected from all rats for analysis by cardiac puncture. Though there were instances when serum chemistry concentrations were higher on injections with both B. bacteriovorus and P. multocida, compared with rats injected with only P. multocida or the controls, findings showed that B. bacteriovorus injected into rats which had previously been injected with P. multocida led to lower levels of alanine aminotransferase, aspartate aminotransferase and creatinine when compared with concentrations in rats injected with only P. multocida. Mortality was reduced by 88% in rats injected with P. multocida and B. bacteriovorus compared with those injected with only P. multocida. It is concluded that B. bacteriovorus effectively mitigated damage caused by P. multocida in rats.
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Jie, Jie, Xiaoyan Xu, Jinjun Xia, et al. "Memory Impairment Induced by Borna Disease Virus 1 Infection is Associated with Reduced H3K9 Acetylation." Cellular Physiology and Biochemistry 49, no. 1 (2018): 381–94. http://dx.doi.org/10.1159/000492890.
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Background/Aims: Borna disease virus 1 (BoDV-1) infection induces cognitive impairment in rodents. Emerging evidence has demonstrated that Chromatin remodeling through histone acetylation can regulate cognitive function. In the present study, we investigated the epigenetic regulation of chromatin that underlies BoDV-1-induced cognitive changes in the hippocampus. Methods: Immunofluorescence assay was applied to detect BoDV-1 infection in hippocampal neurons and Sprague-Dawley rats models. The histone acetylation levels both in vivo and vitro were assessed by western blots. The acetylation-regulated genes were identified by ChIP-seq and verified by RT-qPCR. Cognitive functions were evaluated with Morris Water Maze test. In addition, Golgi staining, and electrophysiology were used to study changes in synaptic structure and function. Results: BoDV-1 infection of hippocampal neurons significantly decreased H3K9 histone acetylation level and inhibited transcription of several synaptic genes, including postsynaptic density 95 (PSD95) and brain-derived neurotrophic factor (BDNF). Furthermore, BoDV-1 infection of Sprague Dawley rats disrupted synaptic plasticity and caused spatial memory impairment. These rats also exhibited dysregulated hippocampal H3K9 acetylation and decreased PSD95 and BDNF protein expression. Treatment with the HDAC inhibitor, suberanilohydroxamic acid (SAHA), attenuated the negative effects of BoDV-1. Conclusion: Our results demonstrate that regulation of H3K9 histone acetylation may play an important role in BoDV-1-induced memory impairment, whereas SAHA may confer protection against BoDV-1-induced cognitive impairments. This study finds important mechanism of BoDV-1 infection disturbing neuronal synaptic plasticity and inducing cognitive dysfunction from the perspective of histone modification.
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Wang, Yiyan, Xiaoheng Li, Fei Ge, et al. "Platelet-derived growth factor BB stimulates differentiation of rat immature Leydig cells." Journal of Molecular Endocrinology 60, no. 1 (2018): 29–43. http://dx.doi.org/10.1530/jme-17-0222.
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Platelet-derived growth factor (PDGF) is one family of growth factors that regulate cell growth and differentiation. Rat Leydig cells express PDGF-β receptor (PDGFRB) during pubertal development. However, the mechanism of PDGF in the regulation of Leydig cell development is unclear. In the present study, rat immature Leydig cells were isolated from the testes of 35-day-old Sprague-Dawley rats and treated with 1 and 10 ng/mL of PDGF-BB. After 24 h of treatment, these cells were harvested for genomics profiling and the medium steroids were measured. 1 and 10 ng/mL PDGF-BB significantly increased androgen production by rat immature Leydig cells. Genomics profiling analysis showed that the expression levels of steroidogenic acute regulatory protein (Star) were increased by 2-fold. Further analysis showed thatFosexpression level was increased 2- and 5-fold by 1 and 10 ng/mL PDGF-BB, respectively. In conclusion, PDGF-BB stimulated the differentiation of rat immature Leydig cells via regulatingStar.
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Mensah, E. A., N. M. Kumar, L. Nielsen, and J. S. Lwebuga-Mukasa. "Distribution of alveolar type II cells in neonatal and adult rat lung revealed by RT-PCR in situ." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 1 (1996): L178—L185. http://dx.doi.org/10.1152/ajplung.1996.271.1.l178.
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Type II pneumocytes in newborn lungs are more uniformly distributed, whereas in adult lungs they are located at alveolar corners. We used morphometry and reverse transcription-polymerase chain reaction in situ hybridization of surfactant protein C mRNA to determine the patterns of type II cell distribution in random lung sections from Sprague-Dawley rats at various neonatal stages and adults. There was a progressive increase in the percentage of type II cells at alveolar corners from 30% at 1 day to 51, 62, 78, and 81% at 3, 5, and 7 days old and adult rats, respectively. There were statistically significant differences (P < 0.001) in the localization of type II cells from the nearest alveolar corner in the 1-day-old compared with 7-day-old and adult rat lungs. These results show that rat type II cells localize to the alveolar corners within the first 7 days postnatally and provide a system for study of factors that regulate alveolar epithelial cell distribution.
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Zhong, Cisheng, Zhang Yu, Wenqian Yu, and Yiping Ling. "Atrial specific granules: The intracellular calcium store." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 2 (1990): 162–63. http://dx.doi.org/10.1017/s0424820100134405.
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It is well known that certain organells in cytosol contain high calcium concentration and they are named intracellular Ca stores. These stores regulate the intracellular Ca concentration. The present project aims at exploring whether the release of atrial natriuretic peptide (ANP) from the atrial specific granules(ASG) is dependent on the release of calcium from the ASG. For this purpose, we have to know first whether the ASG contain high Ca concentration. In this work, positive results were obtained by quantitative electron probe x ray microanalysis (EPMA) and Ca-ATPase cytochemical localization.Adult female Sprague Dawley rats were used. The auricle samples were prepared in five different procedures: 1 )preparation of routine ultrathin sections; 2)ethanolic phosphotungstic acid(EPTA) staining ultrathin sections for ASG showing; [1] 3) cytochemical localization of Ca-ATPase ;[2] 4) preparation of ultrathin cryosections of fresh rapid frozen auricles; [3] 5) quantitative EPMA with Link AN10000 and Link Quantem/FLS quantitative analysis software.
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Shillabeer, G., J. M. Forden, J. C. Russell, and D. C. Lau. "Paradoxically slow preadipocyte replication and differentiation in corpulent rats." American Journal of Physiology-Endocrinology and Metabolism 258, no. 2 (1990): E368—E376. http://dx.doi.org/10.1152/ajpendo.1990.258.2.e368.
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We have investigated the in vitro rate of replication and differentiation of preadipocytes derived from lean (+/+) and obese (cp/cp) male JCR:LA-corpulent (cp) rats in an attempt to identify mechanisms that regulate adipose tissue growth. Cp/cp rats were twofold heavier than age-matched lean rats by 9-10 mo. Cp/cp-derived preadipocytes demonstrated an inherently slower rate of replication than +/+ preadipocytes (population doubling time: cp/cp 52.3 +/- 9.6 h vs. +/+ 19.7 +/- 1.6 h), although the preadipocyte pool in the cp/cp was significantly greater. Cp/cp preadipocytes were resistant to hormonally induced differentiation (19.9 +/- 9.4% of cells accumulated lipid) but differentiated when cocultured with mature adipocytes to the same extent as preadipocytes derived from Sprague-Dawley (SD) rats (cp/cp 48.4 +/- 15.2% vs. SD 52.2 +/- 11.9%). In contrast, SD preadipocytes did not differentiate in response to mature adipocytes from +/+ rats (13.8 +/- 5.2%). Our observations suggest that preadipocyte replication and maturation may not be controlled in a coordinated manner.
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Kim, Jinhyung, Sang Baek Ryu, Sung Eun Lee, et al. "Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?" Journal of Neurosurgery 124, no. 3 (2016): 866–76. http://dx.doi.org/10.3171/2015.1.jns14891.
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OBJECT Neuropathic pain is often severe. Motor cortex stimulation (MCS) is used for alleviating neuropathic pain, but the mechanism of action is still unclear. This study aimed to understand the mechanism of action of MCS by investigating pain-signaling pathways, with the expectation that MCS would regulate both descending and ascending pathways. METHODS Neuropathic pain was induced in Sprague-Dawley rats. Surface electrodes for MCS were implanted in the rats. Tactile allodynia was measured by behavioral testing to determine the effect of MCS. For the pathway study, immunohistochemistry was performed to investigate changes in c-fos and serotonin expression; micro-positron emission tomography (mPET) scanning was performed to investigate changes of glucose uptake; and extracellular electrophysiological recordings were performed to demonstrate brain activity. RESULTS MCS was found to modulate c-fos and serotonin expression. In the mPET study, altered brain activity was observed in the striatum, thalamic area, and cerebellum. In the electrophysiological study, neuronal activity was increased by mechanical stimulation and suppressed by MCS. After elimination of artifacts, neuronal activity was demonstrated in the ventral posterolateral nucleus (VPL) during electrical stimulation. This neuronal activity was effectively suppressed by MCS. CONCLUSIONS This study demonstrated that MCS effectively attenuated neuropathic pain. MCS modulated ascending and descending pain pathways. It regulated neuropathic pain by affecting the striatum, periaqueductal gray, cerebellum, and thalamic area, which are thought to regulate the descending pathway. MCS also appeared to suppress activation of the VPL, which is part of the ascending pathway.
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Franzén, Stephanie, Liselotte Pihl, Angelica Fasching, and Fredrik Palm. "Intrarenal activation of endothelin type B receptors improves kidney oxygenation in type 1 diabetic rats." American Journal of Physiology-Renal Physiology 314, no. 3 (2018): F439—F444. http://dx.doi.org/10.1152/ajprenal.00498.2017.
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About one-third of patients with type 1 diabetes develops kidney disease. The mechanism is largely unknown, but intrarenal hypoxia has been proposed as a unifying mechanism for chronic kidney disease, including diabetic nephropathy. The endothelin system has recently been demonstrated to regulate oxygen availability in the diabetic kidney via a pathway involving endothelin type A receptors (ETA-R). These receptors mainly mediate vasoconstriction and tubular sodium retention, and inhibition of ETA-R improves intrarenal oxygenation in the diabetic kidney. Endothelin type B receptors (ETB-R) can induce vasodilation of the renal vasculature and also regulate tubular sodium handling. However, the role of ETB-R in kidney oxygen homeostasis is unknown. The effects of acute intrarenal ETB-R activation (sarafotoxin 6c for 30–40 min; 0.78 pmol/h directly into the renal artery) on kidney function and oxygen metabolism were investigated in normoglycemic controls and insulinopenic male Sprague-Dawley rats administered streptozotocin (55 mg/kg) 2 wk before the acute experiments. Intrarenal activation of ETB-R improved oxygenation in the hypoxic diabetic kidney. However, the effects on diabetes-induced increased kidney oxygen consumption could not explain the improved oxygenation. Rather, the improved kidney oxygenation was due to hemodynamic effects increasing oxygen delivery without increasing glomerular filtration or tubular sodium load. In conclusion, increased ETB-R signaling in the diabetic kidney improves intrarenal tissue oxygenation due to increased oxygen delivery secondary to increased renal blood flow.
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Yingst, Douglas R., Ali Araghi, Tabitha M. Doci, Raymond Mattingly, and William H. Beierwaltes. "Decreased renal perfusion rapidly increases plasma membrane Na-K-ATPase in rat cortex by an angiotensin II-dependent mechanism." American Journal of Physiology-Renal Physiology 297, no. 5 (2009): F1324—F1329. http://dx.doi.org/10.1152/ajprenal.90363.2008.
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To understand how rapid changes in blood pressure can regulate Na-K-ATPase in the kidney cortex, we tested the hypothesis that a short-term (5 min) decrease in renal perfusion pressure will increase the amount of Na-K-ATPase in the plasma membranes by an angiotensin II-dependent mechanism. The abdominal aorta of anesthetized Sprague-Dawley rats was constricted with a ligature between the renal arteries, and pressure was monitored on either side during acute constriction. Left renal perfusion pressure was reduced to 70 ± 1 mmHg ( n = 6), whereas right renal perfusion pressure was 112 ± 4 mmHg. In control (nonconstricted) rats ( n = 5), pressure to both kidneys was similar at 119 ± 6 mmHg. After 5 min of reduced perfusion, femoral venous samples were taken for plasma renin activity (PRA) and the kidneys excised. The cortex was dissected, minced, sieved, and biotinylated. Lower perfusion left kidneys showed a 41% increase ( P < 0.003) in the amount of Na-K-ATPase in the plasma membrane compared with right kidneys. In controls, there was no difference in cell surface Na-K-ATPase between left and right kidneys ( P = 0.47 ). PRA was 57% higher in experimental animals compared with controls. To test the role of angiotensin II in mediating the increase in Na-K-ATPase, we repeated the experiments ( n = 6) in rats treated with ramiprilat. When angiotensin-converting enzyme was inhibited, the cell surface Na-K-ATPase of the two kidneys was equal ( P =0.46 ). These results confirm our hypothesis: rapid changes in blood pressure regulate trafficking of Na-K-ATPase in the kidney cortex.
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Gohar, Eman Y., Malgorzata Kasztan, Bryan K. Becker, Joshua S. Speed, and David M. Pollock. "Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis." American Journal of Physiology-Renal Physiology 313, no. 2 (2017): F361—F369. http://dx.doi.org/10.1152/ajprenal.00098.2017.
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We recently reported that natriuresis produced by renal medullary salt loading is dependent on endothelin (ET)-1 and purinergic (P2) receptors in male rats. Because sex differences in ET-1 and P2 signaling have been reported, we decided to test whether ovarian sex hormones regulate renal medullary ET-1 and P2-dependent natriuresis. The effect of medullary NaCl loading on Na+ excretion was determined in intact and ovariectomized (OVX) female Sprague-Dawley rats with and without ET-1 or P2 receptor antagonism. Isosmotic saline (284 mosmol/kgH2O) was infused in the renal medullary interstitium of anesthetized rats during a baseline urine collection period, followed by isosmotic or hyperosmotic saline (1,800 mosmol/kgH2O) infusion. Medullary NaCl loading significantly enhanced Na+ excretion in intact and OVX female rats. ETA+B or P2 receptor blockade did not attenuate the natriuretic effect of medullary NaCl loading in intact females, whereas ETA+B or P2 receptor blockade attenuated the natriuretic response to NaCl loading in OVX rats. Activation of medullary P2Y2 and P2Y4 receptors by UTP infusion had no significant effect in intact females but enhanced Na+ excretion in OVX rats. Combined ETA+B receptor blockade significantly inhibited the natriuretic response to UTP observed in OVX rats. These data demonstrate that medullary NaCl loading induces ET-1 and P2-independent natriuresis in intact females. In OVX, activation of medullary P2 receptors promotes ET-dependent natriuresis, suggesting that ovarian hormones may regulate the interplay between the renal ET-1 and P2 signaling systems to facilitate Na+ excretion.
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Sun, Wenjing, Yan Guo, Shirong Zhang, et al. "Fecal Microbiota Transplantation Can Alleviate Gastrointestinal Transit in Rats with High-Fat Diet-Induced Obesity via Regulation of Serotonin Biosynthesis." BioMed Research International 2018 (October 2, 2018): 1–9. http://dx.doi.org/10.1155/2018/8308671.
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Aim. We tested the hypothesis that fecal microbiota transplantation (FMT) could regulate the biotransformation of bile acids, such as deoxycholic acid (DCA) and cholic acid (CA), which in turn regulate the biosynthesis of serotonin in the gut and relieve gastrointestinal dysmotility in high-fat diet- (HFD-) induced obesity in rats. Methods. Male Sprague-Dawley rats were randomly divided into the control diet group, HFD group, and HFD-fed with receiving FMT. HFD was fed for 12 weeks. At the end of two-week HFD, FMT was carried out for two weeks. The gastrointestinal transit, serotonin concentration, the expression of tryptophan hydroxylase 1 (TPH1) and serotonin reuptake transporter (SERT), and the levels of bile acids in intestinal contents were examined. Results. Compared with the control group, the gastrointestinal transit and small intestinal serotonin concentration of HFD-fed rats were increased. In HFD-fed rats, TPH1 protein expression was increased significantly, while SERT protein expression was decreased, but not significant. The levels of CA and DCA in intestinal contents were also significantly increased in HFD-fed rats compared with the control group. After HFD-fed rats receiving FMT treatment, the gastrointestinal transit, small intestinal serotonin concentration, and TPH1 expression were decreased, while SERT expression was not affected. Moreover, the levels of CA and DCA in intestinal contents were also decreased. Conclusions. FMT could alleviate small intestinal transit in the HFD-fed rats by regulating the serotonin biosynthesis. In this process, CA and DCA may be related to the regulation of synthesis of serotonin.
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Liu, Yanping, David R. Harder, and Julian H. Lombard. "Interaction of myogenic mechanisms and hypoxic dilation in rat middle cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2276—H2281. http://dx.doi.org/10.1152/ajpheart.00635.2002.
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The goal of this study was to determine how myogenic responses and vascular responses to reduced Po 2 interact to determine vascular smooth muscle (VSM) transmembrane potential and active tone in isolated middle cerebral arteries from Sprague-Dawley rats. Stepwise elevation of transmural pressure led to depolarization of the VSM cells and myogenic constriction, and reduction of the O2concentration of the perfusion and superfusion reservoirs from 21% O2 to 0% O2 caused vasodilation and VSM hyperpolarization. Myogenic constriction and VSM depolarization in response to transmural pressure elevation still occurred at reduced Po 2. Arterial dilation in response to reduced Po 2 was not impaired by pressure elevation but was significantly reduced at the lowest transmural pressure (60 mmHg). However, the magnitude of VSM hyperpolarization was unaffected by transmural pressure elevation. This study demonstrates that myogenic activation in response to transmural pressure elevation does not override hypoxic relaxation of middle cerebral arteries and that myogenic responses and hypoxic relaxation can independently regulate vessel diameter despite substantial changes in the other variable.
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Gratton, Robert J., Robin E. Gandley, John F. McCarthy, Walter K. Michaluk, Bryan K. Slinker, and Margaret K. McLaughlin. "Contribution of vasomotion to vascular resistance: a comparison of arteries from virgin and pregnant rats." Journal of Applied Physiology 85, no. 6 (1998): 2255–60. http://dx.doi.org/10.1152/jappl.1998.85.6.2255.
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Intrinsic oscillatory activity, or vasomotion, within the microcirculation has many potential functions, including modulation of vascular resistance. Alterations in oscillatory activity during pregnancy may contribute to the marked reduction in vascular resistance. The purpose of this study was 1) to mathematically model the oscillatory changes in vessel diameter and determine the effect on vascular resistance and 2) to characterize the vasomotion in resistance arteries of pregnant and nonpregnant (virgin) rats. Mesenteric arteries were isolated from Sprague-Dawley rats and studied in a pressurized arteriograph. Mathematical modeling demonstrated that the resistance in a vessel with vasomotion was greater than that in a static vessel with the same mean radius. During constriction with the α1-adrenergic agonist phenylephrine, the amplitude of oscillation was less in the arteries from pregnant rats. We conclude that vasomotor activity may provide a mechanism to regulate vascular resistance and blood flow independent of static changes in arterial diameter. During pregnancy the decrease in vasomotor activity in resistance arteries may contribute to the reduction in peripheral vascular resistance.
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Smith, Pauline M., Veronique Mollaret, and Alastair V. Ferguson. "Leptin acts in the rat hypothalamic paraventricular nucleus to induce gastric mucosal damage." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 6 (1998): R2081—R2084. http://dx.doi.org/10.1152/ajpregu.1998.275.6.r2081.
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Leptin is produced and secreted by adipocytes to regulate body weight homeostasis. Leptin acts centrally to reduce weight by decreasing food intake and increasing energy expenditure. The paraventricular nucleus (PVN) is a central nervous system structure suggested as a site at which leptin acts to exert its central effects. Leptin microinjection (10−6 M, 0.5 μl) into the PVN of urethan-anesthetized male Sprague-Dawley rats (150–300 g) resulted in significant gastric damage (mean score = 1.75, n = 16). Damage scores were significantly different than those observed after saline microinjection into the PVN (mean score = 0.00, n = 5, P < 0.05), or leptin microinjection into non-PVN sites (mean score = 0.33, n = 6, P < 0.05). There were no changes in blood pressure (mean area under curve = 401.9 ± 224.2 mmHg * s, n = 11, P > 0.05) or heart rate (mean area under curve = 40.9 ± 25.9 beats, n= 10, P > 0.05) in response to leptin microinjection into PVN. These results suggest that leptin acts on a functionally specific population of PVN neurons involved in the control of gastrointestinal function.
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Titze, Jens, Mehdi Shakibaei, Markus Schafflhuber, et al. "Glycosaminoglycan polymerization may enable osmotically inactive Na+ storage in the skin." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (2004): H203—H208. http://dx.doi.org/10.1152/ajpheart.01237.2003.
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Osmotically inactive skin Na+ storage is characterized by Na+ accumulation without water accumulation in the skin. Negatively charged glycosaminoglycans (GAGs) may be important in skin Na+ storage. We investigated changes in skin GAG content and key enzymes of GAG chain polymerization during osmotically inactive skin Na+ storage. Female Sprague-Dawley rats were fed a 0.1% or 8% NaCl diet for 8 wk. Skin GAG content was measured by Western blot analysis. mRNA content of key dermatan sulfate polymerization enzymes was measured by real-time PCR. The Na+ concentration in skin was determined by dry ashing. Skin Na+ concentration during osmotically inactive Na+ storage was 180–190 mmol/l. Increasing skin Na+ coincided with increasing GAG content in cartilage and skin. Dietary NaCl loading coincided with increased chondroitin synthase mRNA content in the skin, whereas xylosyl transferase, biglycan, and decorin content were unchanged. We conclude that osmotically inactive skin Na+ storage is an active process characterized by an increased GAG content in the reservoir tissue. Inhibition or disinhibition of GAG chain polymerization may regulate osmotically inactive Na+ storage.
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Edgett, Brittany A., Melanie L. Fortner, Arend Bonen, and Brendon J. Gurd. "Mammalian target of rapamycin pathway is up-regulated by both acute endurance exercise and chronic muscle contraction in rat skeletal muscle." Applied Physiology, Nutrition, and Metabolism 38, no. 8 (2013): 862–69. http://dx.doi.org/10.1139/apnm-2012-0405.
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This study examined changes in the expression of translation initiation regulatory proteins and mRNA following both an acute bout of endurance exercise and chronic muscle contractile activity. Female Sprague Dawley rats ran for 2 h at 15 m·min−1 followed by an increase in speed of 5 m·min−1 every 5 min until volitional fatigue. The red gastrocnemius muscle was harvested from nonexercised animals (control; n = 6) and from animals that exercised either immediately after exercise (n = 6) or following 3 h of recovery from exercise (n = 6). Compared with control, ribosomal protein S6 (rpS6) mRNA was elevated (p < 0.05) at both 0 h (+32%) and 3 h (+47%). Both a catalytic subunit of eukaryotic initiation factor 2B (eIF2Bε) (+127%) and mammalian target of rapamycin (mTOR) mRNA (+44%) were increased at 3 h, compared with control. Phosphorylation of mTOR (+40%) and S6 kinase 1 (S6K1) (+266%) were increased immediately after exercise (p < 0.05). Female Sprague Dawley rats also underwent chronic stimulation of the peroneal nerve continuously for 7 days. The red gastrocnemius muscle was removed 24 h after cessation of the stimulation. Chronic muscle stimulation increased (p < 0.05) mTOR protein (+74%), rpS6 (+31%), and eukaryotic initiation factor 2α (+44%, p = 0.069), and this was accompanied by an increase in cytochrome c (+31%). Increased resting phosphorylation was observed for rpS6 (+51%) (p < 0.05) but not for mTOR or eukaryotic initiation factor 4E binding protein 1. These experiments demonstrate that both acute and chronic contractile activity up-regulate the mTOR pathway and mitochondrial content in murine skeletal muscle. This up-regulation of the mTOR pathway may increase translation efficiency and may also represent an important control point in exercise-mediated mitochondrial biogenesis.
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Banday, Anees A., Andrea Diaz Diaz, and Mustafa Lokhandwala. "Kidney dopamine D1-like receptors and angiotensin 1–7 interaction inhibits renal Na+ transporters." American Journal of Physiology-Renal Physiology 317, no. 4 (2019): F949—F956. http://dx.doi.org/10.1152/ajprenal.00135.2019.
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The role of dopamine D1-like receptors (DR) in the regulation of renal Na+ transporters, natriuresis, and blood pressure is well established. However, the involvement of the angiotensin 1–7 (ANG 1−7)-Mas receptor in the regulation of Na+ balance and blood pressure is not clear. The present study aimed to investigate the hypothesis that ANG 1–7 can regulate Na+ homeostasis by modulating the renal dopamine system. Sprague-Dawley rats were infused with saline alone (vehicle) or saline with ANG 1–7, ANG 1–7 antagonist A-779, DR agonist SKF38393, and antagonist SCH23390. Infusion of ANG 1–7 caused significant natriuresis and diuresis compared with saline alone. Both natriuresis and diuresis were blocked by A-779 and SCH23390. SKF38393 caused a significant, SCH23390-sensitive natriuresis and diuresis, and A-779 had no effect on the SKF38393 response. Concomitant infusion of ANG 1–7 and SKF38393 did not show a cumulative effect compared with either agonist alone. Treatment of renal proximal tubules with ANG 1–7 or SKF38393 caused a significant decrease in Na+-K+-ATPase and Na+/H+ exchanger isoform 3 activity. While SCH23390 blocked both ANG 1–7- and SKF38393-induced inhibition, the DR response was not sensitive to A-779. Additionally, ANG 1–7 activated PKG, enhanced tyrosine hydroxylase activity via Ser40 phosphorylation, and increased renal dopamine production. These data suggest that ANG 1–7, via PKG, enhances tyrosine hydroxylase activity, which increases renal dopamine production and activation of DR and subsequent natriuresis. This study provides evidence for a unidirectional functional interaction between two G protein-coupled receptors to regulate renal Na+ transporters and induce natriuresis.
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Vitulli, William F., Connie P. Anderson, Joseph M. Quinn, and Julie D. Jarvis. "Insulin and Dextrose Effects on Fixed-Interval Behavioral Thermoregulation in Albino Rats." Perceptual and Motor Skills 71, no. 1 (1990): 7–15. http://dx.doi.org/10.2466/pms.1990.71.1.7.
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This study is a systematic replication of the effects of insulin doses on operant behavior reinforced (in an earlier study) by fixed-ratio schedules of microwave (MW) reinforcement. In this study, insulin and dextrose doses were administered (ip) prior to fixed-interval 2-min. schedules of MW reinforcement in rats tested in a cold environment. Six Sprague-Dawley rats were conditioned to regulate their thermal environment with 5-sec. exposures of MW radiation (SAR = 0.34 Watts/kg/(mW/cm2) under the FI-2′ schedules. Humulin-regular insulin and 50% solutions of dextrose were administered (ip) alternately with saline control sessions for 8-hr. durations. A within-subjects, repeated-measures 4 × 8 × 3 factorial analysis of variance design showed that insulin doses suppressed operant responding for heat, which confirmed the results of the earlier study under a different schedule. In addition, high doses of dextrose had similar suppressing effects on operant responding for heat. The data are interpreted in terms of the discriminative properties of increased thermogenesis produced by the insulin and dextrose doses. The suppressing effects were more pronounced for the first two hours, yet they persisted for approximately six hours of the 8-hr. sessions.
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Tang, Peng, Chunguang Duan, Zheng Wang, et al. "NPY and CGRP Inhibitor Influence on ERK Pathway and Macrophage Aggregation during Fracture Healing." Cellular Physiology and Biochemistry 41, no. 4 (2017): 1457–67. http://dx.doi.org/10.1159/000468405.
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Aim: The aims of this study are to investigate the effects of neurotransmitters NPY and CGRP on ERK signaling in fracture healing, and to identify the correlation between macrophage aggregation and fracture healing. Methods: Male Sprague-Dawley rats were used to build a fracture model. The neurotransmitter receptor inhibitors were injected intraperitoneally into the rats. Immunofluorescence staining and ELISA were employed to determine the expression of NPY and CGRP in fracture area and the peripheral blood, respectively. Micro-CT together with histological staining were utilized to assess the fracture healing conditions. Relative protein expression was determined using western blot. Immunofluorescence staining was used to detect the aggregation of macrophages in the injury area. Results: During fracture healing, the serum NPY and CGRP significantly increased. The levels of NPY and CGRP reached a peak in the 8th week and reduced significantly thereafter. NPY and CGRP inhibitors could inhibit fracture healing and down-regulate the phosphorylated ERK. Macrophages (NPY+ and CGRP+) aggregated in the injury area. Conclusion: NPY and CGRP participated in fracture healing, in which they were also shown to influence phosphorylated ERK expression. In addition, macrophages are involved in the fracture healing process.
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Klinger, J. R., D. S. Wrenn, R. R. Warburton, L. Pietras, L. C. Ou, and N. S. Hill. "Atrial natriuretic peptide expression in rats with different pulmonary hypertensive responses to hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (1997): H411—H417. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h411.
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Mechanisms that regulate atrial natriuretic peptide (ANP) expression during hypoxia are not well defined. We hypothesized that plasma immunoreactive ANP (irANP) and right heart irANP and ANP mRNA levels would be greater in a strain of Sprague-Dawley rats that develops more severe hypoxic pulmonary hypertension (H rats) than another strain (M rats). After 3 wk of hypoxia (0.5 atm), right ventricular systolic pressure (RVSP) and the right ventricle (RV) weight-to-left ventricle plus septum (LV (+) S) weight ratio [RV/(LV+S)] were greater in H rats than in M rats (70 +/- 4 vs. 40 +/- 2 mmHg and 0.59 +/- 0.02 vs. 0.50 +/- 0.02, respectively; P < 0.05 for both), but plasma ANP increased twofold and RV irANP and ANP mRNA increased fivefold in both rat strains. After 3 days of normoxic recovery from chronic hypoxia, RVSP, RV/(LV+S), and RV irANP and ANP mRNA levels decreased in M rats but not in H rats. Plasma irANP decreased to baseline levels in both rat strains. We conclude that, in addition to changes in RV pressure and hypertrophy, hypoxia acts through other mechanisms to modulate RV ANP synthesis and circulating ANP levels in hypoxia-adapted rats.
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Penissi, Alicia B., María I. Rudolph, Mariano E. Vera та ін. "Inhibitory Activity of α,β-Unsaturated Lactones on Histamine Release from Rat Peritoneal Mast Cells". Natural Product Communications 3, № 4 (2008): 1934578X0800300. http://dx.doi.org/10.1177/1934578x0800300402.
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The present study was designed to examine the effects of a sesquiterpene lactone isolated from Artemisia douglasiana Besser (dehydroleucodine, DhL), a xanthanolide sesquiterpene isolated from Xanthium cavanillesii Schouw (xanthatin, Xt) and a semisynthetic butenolide (3-benzyloxymethyl-5 H-furan-2-one, But) on mast cell histamine release induced by compound 48/80. Peritoneal mast cells from male adult Sprague-Dawley rats were purified in Percoll, preincubated in the presence of test lactones (DhL, Xt or But) and then challenged with the mast cell activator compound 48/80. Concentration-response studies of mast cell histamine release evoked by compound 48/80, evaluation of mast cell viability and morphology studies by light microscopy were carried out. Biochemical and morphological studies showed the effectiveness of the above lactones to inhibit secretory responses of rat peritoneal mast cells. The present study provides evidence in favor of the hypothesis that DhL, Xt and But inhibit compound 48/80-induced histamine release from rat peritoneal mast cells. Our findings may provide an insight into the design of novel pharmacological agents that may be used to regulate the mast cell response.
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Amiri, F., and R. Garcia. "Differential regulation of renal glomerular and preglomerular vascular angiotensin II receptors." American Journal of Physiology-Endocrinology and Metabolism 270, no. 5 (1996): E810—E815. http://dx.doi.org/10.1152/ajpendo.1996.270.5.e810.
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The activity of the renin-angiotensin system (RAS) can be influenced by sodium intake and angiotensin II (ANG II) infusion. It has been shown that ANG II can regulate the density of its receptors. Therefore, we investigated the regulation of glomerular and preglomerular vascular ANG II receptors by changes in RAS activity. Sprague-Dawley rats were fed a low- or high-sodium diet or were infused with nonpressor or pressor doses of ANG II for 7 days. ANG II receptor characteristics were determined by radioligand binding assays with use of ANG II antagonists losartan and PD-123319. AT1 was the only receptor type found in membrane preparations from all groups. Glomerular ANG II receptor characteristics in all groups were unchanged compared with their controls, whereas vascular receptor density was significantly downregulated by sodium restriction. We conclude that glomerular and preglomerular vascular ANG II receptors are differentially regulated such that AT1 receptors in preglomerular vessels can be regulated by changes in endogenous RAS. ANG II infusion did not induce any modification of either glomerular or vascular AT1 receptors, suggesting a predominant role of the endogenous local renal RAS.
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Chang, Jie, Bing Liu, Yan-xia Cheng, Jin-guang Zhang, Shuo Tao, and Hong-ling Yan. "Effect of Repaglinide on Blood Glucose, Endothelial Function, Lipid Metabolism, and Inflammatory Reaction in a Rat Model of Atherosclerosis." Dose-Response 18, no. 2 (2020): 155932582091876. http://dx.doi.org/10.1177/1559325820918762.
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Objective: To investigate the protective effect of repaglinide on rat with atherosclerosis. Methods: Sprague Dawley (SD) rats were divided into control, model, repaglinide, and metformin groups. In addition to the normal group, rats were given intraperitoneal injection of streptozotocin and high-fat diet (HFD). Meanwhile, repaglinide or metformin was administrated to the treatment rats, respectively, for 4 weeks. Serum, plasma, liver, epididymal fat, and aorta thoracica were obtained to observe the protective effect of repaglinide on rat with atherosclerosis. Results: Compared to the control group, blood glucose was increased in the model group ( P < .05), while it was decreased in the drug-administered groups. In addition, the levels of endothelin 1, TG, TC, low-density lipoprotein cholesterol, atherogenic index, liver index, and epididymal fat index were significantly increased, but the levels of high-density lipoprotein cholesterol, plasminogen activator inhibitor 1, and antiatherogenic index were decreased significantly in the model group compared to the control group ( P < .05, respectively). And these effects were reversed by treatment with repaglinide ( P < .05, respectively). Conclusion: Our results suggested that repaglinide may regulate the formation of early atherosclerosis through the abovementioned mechanisms.
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Liu, Xiaoli, Shanshan Zhang, Chaoyue Xu, et al. "The Protective of Baicalin on Myocardial Ischemia-Reperfusion Injury." Current Pharmaceutical Biotechnology 21, no. 13 (2020): 1386–93. http://dx.doi.org/10.2174/1389201021666200605104540.
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Background: The aim of this study was to explore the inhibitory effect of baicalin on myocardial apoptosis induced by Ischemia-Reperfusion (I/R). Methods: Sprague Dawley rats' heart and myocardial cells I/R model were established in vivo and vitro, then 100 mg/kg and 10 μmol/l baicalin were administrated, respectively. The experiment was randomly divided into 4 groups (n=10): Control; I/R; IR+DMEM; and I/R+baicalin groups. Postoperation, the Left Ventricular (LV) End-Diastolic Pressure (LVEDP), the maximum velocity of LV contraction (dP/dtmax) and the maximum velocity of LV diastole (dP/dtmin) were recorded by the transthoracic echocardiography; the myocardial apoptosis percentage was analyzed by Annexin VFITC/ PI and TUNEL staining, and the apoptosis gene and protein were detected by RT-PCR and western blot. Furthermore, the protein expression of the calcium-sensing receptor (CaSR) and ERK1/2 phosphorylation were observed by western blot and Fura-2-acetoxymethyl ester. Moreover, primary rats’ cardiomyocytes were cultured and ERK1/2 specific inhibitor PD98059 was added to the culture medium. The cell survival rate, vitality and apoptosis were detected by MTT, lactate dehydrogenase (LDH) and TUNEL staining assay Kit, respectively. Results: Our present study showed that baicalin significantly improved LV hemodynamic parameters and myocardial apoptosis in myocardial I/R injury rats. Furthermore, we found that baicalin could down-regulate the protein expression of CaSR, but up-regulate the protein expression of ERK1/2. Furthermore, when the cells were pretreated with ERK1/2 inhibitor PD98059, the cells survival rate significantly decreased, but LDH activity and apoptosis significantly increased. The results indicated that the effect of baicalin on myocardial I/R injury could be inhibited by ERK1/2 inhibitor. Conclusion: In conclusion, our data suggests that baicalin attenuates I/R-induced myocardial injury maybe through the suppression of the CaSR/ERK1/2 signaling pathway.
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Lyra-Leite, Davi M., Allen M. Andres, Andrew P. Petersen, et al. "Mitochondrial function in engineered cardiac tissues is regulated by extracellular matrix elasticity and tissue alignment." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 4 (2017): H757—H767. http://dx.doi.org/10.1152/ajpheart.00290.2017.
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Mitochondria in cardiac myocytes are critical for generating ATP to meet the high metabolic demands associated with sarcomere shortening. Distinct remodeling of mitochondrial structure and function occur in cardiac myocytes in both developmental and pathological settings. However, the factors that underlie these changes are poorly understood. Because remodeling of tissue architecture and extracellular matrix (ECM) elasticity are also hallmarks of ventricular development and disease, we hypothesize that these environmental factors regulate mitochondrial function in cardiac myocytes. To test this, we developed a new procedure to transfer tunable polydimethylsiloxane disks microcontact-printed with fibronectin into cell culture microplates. We cultured Sprague-Dawley neonatal rat ventricular myocytes within the wells, which consistently formed tissues following the printed fibronectin, and measured oxygen consumption rate using a Seahorse extracellular flux analyzer. Our data indicate that parameters associated with baseline metabolism are predominantly regulated by ECM elasticity, whereas the ability of tissues to adapt to metabolic stress is regulated by both ECM elasticity and tissue alignment. Furthermore, bioenergetic health index, which reflects both the positive and negative aspects of oxygen consumption, was highest in aligned tissues on the most rigid substrate, suggesting that overall mitochondrial function is regulated by both ECM elasticity and tissue alignment. Our results demonstrate that mitochondrial function is regulated by both ECM elasticity and myofibril architecture in cardiac myocytes. This provides novel insight into how extracellular cues impact mitochondrial function in the context of cardiac development and disease. NEW & NOTEWORTHY A new methodology has been developed to measure O2 consumption rates in engineered cardiac tissues with independent control over tissue alignment and matrix elasticity. This led to the findings that matrix elasticity regulates basal mitochondrial function, whereas both matrix elasticity and tissue alignment regulate mitochondrial stress responses.