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Статті в журналах з теми "Heart Effect of drugs on":

1
Girouard, Catherine, Jean-Pierre Grégoire, Paul Poirier, and Jocelyne Moisan. "Effect of contraindicated drugs for heart failure on hospitalization among seniors with heart failure." Medicine 96, no. 9 (March 2017): e6239. http://dx.doi.org/10.1097/md.0000000000006239.
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2
Charlton, Matthew, and Jonathan P. Thompson. "Drugs acting on the heart: antihypertensive drugs." Anaesthesia & Intensive Care Medicine 16, no. 5 (May 2015): 227–31. http://dx.doi.org/10.1016/j.mpaic.2015.02.007.
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Charlton, Matthew, and Jonathan Thompson. "Drugs acting on the heart: antihypertensive drugs." Anaesthesia & Intensive Care Medicine 19, no. 7 (July 2018): 365–69. http://dx.doi.org/10.1016/j.mpaic.2018.04.005.
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4
Al-Hashimi, Mhamad, and Jonathan P. Thompson. "Drugs acting on the heart: antihypertensive drugs." Anaesthesia & Intensive Care Medicine 13, no. 8 (August 2012): 369–73. http://dx.doi.org/10.1016/j.mpaic.2012.05.007.
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Ladak, Nadia, and Jonathan Thompson. "Drugs acting on the heart: antihypertensive drugs." Anaesthesia & Intensive Care Medicine 10, no. 8 (August 2009): 392–95. http://dx.doi.org/10.1016/j.mpaic.2009.04.016.
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6
Ritchie, Helen E., Isabelle Broström Huss, and William S. Webster. "The effect of anti-emetic drugs on rat embryonic heart activity." Reproductive Toxicology 87 (August 2019): 140–45. http://dx.doi.org/10.1016/j.reprotox.2019.06.002.
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7
Cohn, Jay N. "Role of drugs for systemic hypertension and their effect on the heart." American Journal of Cardiology 60, no. 12 (October 1987): G72—G74. http://dx.doi.org/10.1016/0002-9149(87)90595-9.
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8
Cesana, F., C. Colombo, C. Valsecchi, M. Stucchi, P. Vallerio, A. Cereda, P. Meani, R. Ricotta, S. Siena, and C. Giannattasio. "P4.20 SHORT-TERM EFFECT OF ANTI-VEGF DRUGS ON HEART AND VESSELS." Artery Research 7, no. 3-4 (2013): 141. http://dx.doi.org/10.1016/j.artres.2013.10.138.
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9
Verdurmen, Kim M. J., Alexandra D. J. Hulsenboom, Judith O. E. H. van Laar, and S. Guid Oei. "Effect of tocolytic drugs on fetal heart rate variability: a systematic review." Journal of Maternal-Fetal & Neonatal Medicine 30, no. 20 (November 2016): 2387–94. http://dx.doi.org/10.1080/14767058.2016.1249844.
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10
Deschodt-Arsac, Véronique, Guillaume Calmettes, Gilles Gouspillou, Richard Rouland, Eric Thiaudiere, Sylvain Miraux, Jean-Michel Franconi, and Philippe Diolez. "System analysis of the effect of various drugs on cardiac contraction energetics." Biochemical Society Transactions 38, no. 5 (September 2010): 1319–21. http://dx.doi.org/10.1042/bst0381319.
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We used MoCA (Modular Control and Regulation Analysis) to demonstrate in intact beating rat heart that physiological activation of contraction by adrenaline involves the almost perfect parallel activation of both mitochondria and myofibrils by intracellular Ca2+. This explains the perfect homoeostasis of the energetic intermediate PCr (phosphocreatine) in heart. When using drugs specifically stimulating either supply or demand activities, MoCA helped reveal the very specific mode of regulation of heart contraction energetics. Only activation of myofibrils activity (demand), either by increasing intracellular Ca2+ concentration or myofibrils sensitivity to Ca2+, triggers activation of contractile activity. In contrast, the activation of mitochondrial activity (supply) has strictly no effect on contraction, either directly or through PCr changes (intermediate).

Дисертації з теми "Heart Effect of drugs on":

1
Maune, Jerene Mary 1953. "THE EFFECT OF CAFFEINE ON HEART RATE, RHYTHM AND BLOOD PRESSURE." Thesis-Reproduction (electronic), The University of Arizona, 1986. http://hdl.handle.net/10150/276372.
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2
Rossouw, Ellen. "The effect of androgenic anabolic steroids on the susceptibility of the rat heart to ischaemia and reperfusion injury." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/53105.
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Thesis (MSc)--University of Stellenbosch, 2002.
ENGLISH ABSTRACT: Background: Athletes use androgenic anabolic steroids (AAS) to enhance their physical performance. The abuse of AAS is however associated with a host of side effects including sudden death due to cardiac arrest. The use of AAS leads to myocardial hypertrophy, which possibly makes the heart more prone to ischaemia/reperfusion injury, since it often develops in the absence of proper vasculature development. Chronic AAS use also disrupts myocardial p-adrenoreceptor function and possibly cAMP, signalling in the heart. Drugs increasing cAMP and decreasing cGMP levels in the ischaemic myocardium exacerbate myocardial ischaemia/reperfusion injury. We also know that AAS causes coronary artery disease secondary to the deleterious alteration of lipid profiles by increasing the LOL cholesterol and decreasing the HOLcholesterol levels. AAS treatment may increase systemic TNFa levels by stimulating lymphocyte TNFa secretion that has been implicated in the depression of myocardial function, myocardial hypertrophy and the worsening of ischaemia/reperfsuion injury. Aims: To determine whether chronic AAS treatment in trained and untrained rats influences: 1) heart function and susceptibility to ischaemia/reperfusion injury, 2) myocardial cyclic nucleotide levels (cAMP and cGMP) and 3) myocardial TNFa levels. Material and methods: Male Sprague-Dawley rats (n=100) were divided into 4 groups: sedentary vehicle (placebo) treated group, sedentary AAS treated group, exercise vehicle (placebo) treated group, and exercise AAS treated group. Steroid treated animals received an intramuscular injection of nandrolone laureate (0.375 mg/kg) once a week, for six weeks. Training consisted of swim sessions 6 days a week for 6 weeks. Swim time was incrementally increased up to a maximum of 50 minutes a day. For biometric parameters heart weight and body weight were documented. Hearts were mounted on a l.anqendorff perfusion apparatus and left ventricular developed pressure (LVDP), heart rate (HR) and coronary flow (CF) was monitored. The hearts were subjected to a period of 20 minutes of global ischaemia, followed by 30 minutes of reperfusion. Functional parameters was again monitored and documented. For biochemical analysis, blood was collected for the determination of serum lipid levels and myocardial tissue samples were collected before, during and after ischaemia for the determination of myocardial TNFa, cGMP and cAMP levels and p38 activity. Conclusions: Results obtained would suggest that AAS exacerbate exercise induced myocardial hypertrophy. It also prevents the exercise-induced improvement in cardiac function. AAS use reduces reperfusion function in treated hearts, which may suggest that AAS exacerbates ischaemie and reperfusion injury. Furthermore it was seen that AAS elevates basal (preischaemie) cyclic nucleotide levels and basal (pre-ischaemic) as well as reperfusion TNFa levels. This may also contribute to the exacerbation of ischaemic and reperfusion injury.
AFRIKAANSE OPSOMMING: Agtergrond: Androgeniese anaboliese steroïede (AAS) word dikwels deur atlete gebruik om sportprestasie te verbeter. Die misbruik van AAS het egter talle newe effekte, insluitende skielike dood wat gewoonlik toegeskryf word aan hartaanvalle. Die gebruik van AAS lei onder andere tot miokardiale hipertrofie wat opsigself, as gevolg van ontoereikende vaskulêre ontwikkeling tydens die ontwikkeling van hipertrofie, die hart nog meer vatbaar vir isgemie/herperfusie skade maak. Kroniese AAS toediening versteur miokardiale beta-adtenoresepter funksie en moontlik die tweede boodskapper, sAMP, seintransduksie in die hart. Ons weet ook dat AAS koronêre hartvatsiektes veroorsaak. Laasgenoemde is sekondêr tot die nadelige lipiedprofiel verandering, wat 'n verhoging in LDL-C en 'n verlaging in HDL-C insluit. Middels wat miokardiale sAMP vlakke verhoog en sGMP vlakke in die isgemiese miokardium verlaag, vererger miokardiale isgemie/herperfusie skade. AAS behandeling kan moontlik ook sistemiese TNFa vlakke verhoog deur limfosiet TNFa sekresie te stimuleer. Die verhoogde TNFa vlakke word verbind aan die onderdrukking van miokardiale funksie, miokardiale hipertrofie en die verergering van isgemie/herperfusie skade. Doelwitte: Die doelwitte van die studie was om te bepaal of kroniese AAS toediening in geoefende en ongeoefende rotte 1) hartfunksie en die hart se vatbaarheid vir isgemie/herperfusie skade beïnvloed, 2) miokardiale sikliese nukleotiedvlakke (sAMP en sGMP) beïnvloed en 3) miokardiale TNFa-vlakke beïnvloed. Materiale en metodes: Manlike Sprague-Dawley rotte (n=100) is gebruik en in 4 groepe verdeel: 'n ongeoefende placebo groep (kontrole); 'n ongeoefende steroïedbehandelde groep; 'n geoefende placebo groep (kontrole) en 'n geoefende steroïedbehandelde groep. Steroïed behandelde diere het 'n intramuskulêre nandroloon lauraat inspuiting (0.375 mg/kg) een keer per week vir ses weke ontvang. Die oefenprogram het bestaan uit ses swemsessies 'n week vir ses weke. Die swemtyd is geleidelik weekliks verhoog tot by 'n maksimum tyd 50 min. Die waterbadtemperatuur is tussen 30 - 32 oe gehandhaaf. Vir biometriese parameters is hartgewig en liggaamsgewig genoteer. Harte is op 'n Langendorff perfusie apparaat gemonteer en linker ventrikulêre ontwikkelde druk (LVOD), koronêre vloei (KV) en harttempo (HT) is genoteer. Die harte is vervolgens blootgestel aan 20 minute van globale isgemie gevolg deur 'n 30 minute herperfusieperiode. LVOD, KV en HT is weer eens noteer. Vir biochemiese doeleindes is bloed voor perfusie versamelom serum lipied vlakke te bepaal. Miokardiale weefsel is versamel voor, tydens en na isgemie vir die bepaling van TNFa, cGMP en AMP vlakke asook p38 aktiwiteit. Gevolgtrekkings: Na aanleiding van resultate verkry wil dit voorkom asof die gebruik van steroïde oefeningsgeïnduseerde miokardiale hipertrofie vererger. Dit verhoed ook oefeningsgeïnduseerde verbetering in miokardiale funksie. AAS lei tot 'n verlaagde herperfusiefunksie in behandelde harte, wat dalk mag dui op MS verergering van isgemie en herperfusie skade. Verder was daar ook waargeneem dat MS basale (pre-isgemiese) sikliese nukleotiedvlakke en basale TNFa-vlakke sowel as herperfusie TNFa vlakke verhoog. Die verhoging in TNF-a vlakke mag dus moontlik ook bydra tot die verergering van isgemie- en herperfusieskade.
3
Kalis, Joni Kathryn. "THE EFFECT OF BETA-ADRENERGIC BLOCKADE ON THE DRIFT IN OXYGEN CONSUMPTION WITH PROLONGED EXERCISE." Thesis-Reproduction (electronic), The University of Arizona, 1985. http://hdl.handle.net/10150/292014.
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Elliott-Pearce, Ruth Ann. "The effect of drugs on isolated detrusor muscle contraction." Electronic Thesis or Dissertation, University of Leicester, 1996. http://hdl.handle.net/2381/34339.
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Detrusor instability is the commonest type of urinary incontinence in the elderly and is present in up to 50% of patients attending continence clinics. Treatment of this condition, aimed at reducing uncontrollable detrusor contractions, is at present unsatisfactory. For example, calcium antagonists are cliniclly disappointing and studies were carried out to investigate why they are ineffective. Rats were treated with nimodipine for 8 days or with a single dose. Treatment for 8 days had no effect on isolated detrasor contraction but a single dose reduced detrasor contractile response. It is propossed that chronic treatment with nimodipine caused an up-regulation of calcium channels as a compensatory mechanism. Oestrogens have been shown to have an inhibitory effect on detrusor muscle contraction after in vitro and in vivo treatment. In post-menopausal women with a uterus unopposed oestrogens should not be given, but progesterone has anti-oestrogenic actions. When rats were treated with oestrogen and progesterone for 8 days, there was no effect on rat detrasor contractile response. An anti-oestrogenic effect of progesterone has therefore been demonstrated in rat detrusor smooth muscle. Caffeine has been shown to increase detrasor pressme on bladder filling in patients with detrusor instability. The effect of low concentrations of caffeine on the contractile response of isolated human and rat detrusor muscle was therefore determined. Caffeine was found to have only a slight potentiating effect on isolated human and rat detruosr muscle contraction. The results in this thesis have important clinical imphcations for the treatment of detrusor instability. It may be more effective to administer calcium antagonists in an intermittent manner. Oestrogens are better given alone or with the lowest possible dose of progestogens. Caffeine would not be contraindicated in patients with detrusor instability.
5
Komulainen, S. (Silja). "Effect of antihypertensive drugs on blood pressure during exposure to cold:experimental study in normotensive and hypertensive subjects." DoctoralThesis, University of Oulu, 2010. http://urn.fi/urn:isbn:9789514286131.
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Abstract The aim of the present study was to describe the effects of different types of cold exposures on blood pressure (BP) and heart rate (HR) and to test how these cold-induced effects are modulated by antihypertensive drugs representing different kind of mechanisms of action. The tested drugs represented the following antihypertensive drug subgroups: metoprolol from beta-blocking agents, carvedilol from alfa- and beta-blocking agents, lisinopril from angiotensin converting enzyme inhibitors, eprosartan from angiotensin II antagonists, amlodipine from calcium channel blockers and hydrochlorothiazide from diuretics. The main outcome measures were the levels and changes in systolic (SBP) and diastolic blood pressure (DBP) and HR before, during and after cold exposure. The normotensive and mildly hypertensive subjects were exposed either to –15°C for 15 minutes (with winter clothing), 5°C for 45 minutes (minimal clothing) or to a cold pressor test (CPT). Before measurements at –15°C, metoprolol, carvedilol, lisinopril, eprosartan, hydrochlorothiazide or placebo were given for a week in a double-blind and crossover manner. In one test procedure (5°C and CPT) the test subjects ingested amlodipine for three days or were without drug ingestion before the tests in a crossover manner. Both SBP and DBP were markedly increased by all types of cold exposure. Cold-induced rises of SBP/DBP were higher during the exposure to 5°C and –15°C (19–35/20–24 mmHg) than during CPT (13/16 mmHg). Metoprolol, carvedilol, lisinopril, eprosartan and amlodipine decreased the level of BP during the exposure to 5°C and –15°C compared to placebo or no drug. The antihypertensive drugs, with dosages used in this study, did not affect the cold-induced rise of BP compared to no drug or placebo. HR increased during CPT, but decreased during exposure to 5°C and –15°C. Metoprolol and carvedilol decreased HR during exposure to –15°C compared to placebo. The present study demonstrates for the first time the effects of antihypertensive drugs on BP in hypertensive subjects exposed to cold similar to normal outdoor exposure in winter. Although the magnitude of the cold-induced rise in BP was not affected by the drugs, the drug-induced decrease in the level of BP kept the peak values in the cold closer to the recommended threshold limit values
Tiivistelmä Tutkimuksen tarkoituksena oli selvittää eri mekanismeilla vaikuttavien verenpainelääkkeiden vaikutusta verenpainevasteisiin ja sydämen lyöntitiheyteen kylmässä sekä verrata erilaisten kylmäaltistusten vaikutusta verenpaineeseen ja sydämen lyöntitiheyteen. Tutkitut lääkkeet edustivat seuraavia verenpainelääkeryhmiä: metoprololi beetasalpaajia, karvediloli yhdistettyjä alfa- ja beetasalpaajia, lisinopriili ACE-estäjiä, eprosartaani angiotensiini II antagonisteja, amlodipiini kalsiumestäjiä ja hydroklooritiatsidi diureetteja. Tärkeimmät mitatut vasteet olivat systolisen ja diastolisen verenpaineen ja sydämen lyöntitiheyden tasot ja muutokset ennen kylmäaltistusta, kylmäaltistuksen aikana ja sen jälkeen. Lisäksi mitattiin lämpötilavasteita ja tuntemuksia. Normo- ja hypertensiiviset koehenkilöt altistettiin joko –15°C:seen 15 minuutin ajaksi (talvivaatetuksessa), 5°C:seen 45 minuutin ajaksi (minimaalisella vaatetuksella) tai tehtiin ns. käden kylmävesitesti (CPT). Testisarjoissa (–15°C) metoprololi, karvediloli, lisinopriili, eprosartaani ja hydroklooritiatsidi tai plasebo annettiin viikon ajan kaksoissokko- ja vaihtovuoromenetelmällä. Yhdessä testisarjassa (5°C ja CPT) koehenkilöt ottivat amlodipiinia 3 päivän ajan tai olivat ilman lääkettä ennen testikertoja vaihtovuoroisessa järjestyksessä. Kaikki kylmäaltistustyypit nostivat merkittävästi sekä systolista että diastolista verenpainetta. Systolisen ja diastolisen verenpaineen nousu oli korkeampi koko kehon kylmäaltistuksissa (5°C tai –15°C) (19–35/20–24 mmHg) kuin ns. kylmävesitestissä (13/16 mmHg). Metoprololi, karvediloli, lisinopriili, eprosartaani ja amlodipiini laskivat verenpaineen tasoja koko kehon kylmäaltistuksessa verrattuna plaseboon. Yksikään verenpainelääkkeistä ei vaikuttanut merkittävästi kylmän aiheuttamaan verenpaineen nousuun verrattuna tutkimuskertaan ilman lääkettä tai plaseboon. Sydämen lyöntitiheys nousi ns. kylmävesitestin aikana, mutta laski koko kehon kylmäaltistuksissa (5°C ja –15°C). Metoprololi ja karvediloli laskivat sydämen lyöntiheyttä kylmäaltistuksessa (–15°C) verrattuna plaseboon. Tämä tutkimus kuvaa ensimmäistä kertaa, kuinka verenpainelääkkeet vaikuttavat verenpainetasoihin ja -vasteisiin kylmäaltistuksessa, joka simuloi tyypillisiä ulko-olosuhteita talvella. Vaikka lääkkeet eivät estäneet kylmän aiheuttamaa verenpaineen nousua, ne laskivat verenpaineen tasoa, jolloin verenpaine pysyi kylmässäkin lähempänä suositusrajoja
6
Ngamratanapaiboon, Surachai. "Metabolomics investigations of the effect of drugs on mammalian cells." Electronic Thesis or Dissertation, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/41178/.
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Cell-based metabolomics using LC-MS systemizes the study of the uniqueness of small-molecule metabolite (metabolomes) profiles in cellular processes. Cell-based metabolomics can potentially be used in many applications for the study of biological perturbation from stimulants in cellular pathways. The advantages of cell-based metabolomics include ease of control and interpretation when compared to the study of human subjects and animal models. Furthermore, this method can decrease some highly challenging problems that occur in genomics, transcriptomics and proteomics. Nowadays, cell culture in metabolomics studies has been used in many applications. These include cell culture and bioreactor optimisation, phenotype classification, stimulant testing effect, target and toxicity analysis, metabolic networks determination and modelling, and biomarker and drug target discovery. In this study, the reverse phase-liquid chromatography-mass spectrometry and hydrophilic interaction chromatography-mass spectrometry for comprehensive metabolic profiling well suited to the untargeted analysis of non-polar and polar metabolites in mammalian cells were developed, optimized and validated. These methods can separate and detect most of hydrophobic and polar metabolites that are normally found in mammalian cell lines. After that the LC-MS methods were applied to assess the effects of drugs with known and unknown cellular metabolic effects on three mammalian cell lines, namely HMVECs for antipsychotics experiment, MCF-7 cells for cordycepin experiment and MIN6 cells for fluoxetine experiment by using untargeted metabolic profiling. The global effects of antipsychotics at high therapeutic dosage in HMVECs were investigated. The results support for the toxicity hypothesis with measurements that confirm previous findings and reveal the exact biological pathways of antipsychotic-altered BBB functions. It was found that antipsychotics may affect the bioenergetics pathway due to mitochondrial dysfunction resulted in ketoacidosis and inducing oxide stress by reactive oxygen species generation. In the MCF- cell experiment, the results of the untargeted metabolite profiling demonstrated the clear anti-breast cancer effects of cordycepin and pentostatin. By investigating the metabolite profiles, clear synergistic effects of cordycepin and pentostatin combined in comparison to cordycepin activity alone in MCF-7 cells was observed. Furthermore, the pathway analysis indicated that anti-breast cancer activity was mainly responsible for alterations in purine and pyrimidine metabolism and bioenergetics. Additionally, cordycepin may be involved in the inhibition of cell proliferation and differentiation, and the activation of cell apoptosis. The last experiment on MIN6 cells, the developed and optimized HILIC-MS approach in order to determine the biological pathways which are impaired by fluoxetine on glucose-stimulated insulin secretion on MIN6 cell lines was performed. It is found that fluoxetine may impair glycolysis, TCA and fatty acid metabolism on MIN6 cell lines. Moreover, it is also reveal that the alteration of biological pathways on MIN6 cells by known ETC inhibitors (rotenone (Complex I inhibitor) antimycin (Complex III inhibitor)) and azide (a complex IV inhibitor). From comparison with these ETC inhibitors, it is found that fluoxetine may have the same effect pattern with azide.
7
Lange, Jeremy David. "The effect of anti-malarial drugs on the pituitary gland." Electronic Thesis or Dissertation, University of Leeds, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238726.
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8
Hutton, Therese. "The effect of serum on the hypodynamic frog heart." Electronic Thesis or Dissertation, University of Central Lancashire, 1989. http://clok.uclan.ac.uk/21032/.
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An investigation was made of the effects of serum and serum fractions on the isolated spontaneously beating frog heart preparation. Initial experiments were performed to develop a sensitive bioassay preparation to test for inotropic agents in serum. The isolated spontaneously beating frog heart was found to be sensitive, reliable and responded consistently to serum and its components. During the development of the bioassay it was found that the heart became weak after prolonged perfusion. An investigation was then made to determine the mechanism underlying the development of the hypodynamic (weak) condition of the isolated heart. It was found that a heart which was immersed in static oxygenated Ringer's solution did not become hypodynamic. Continuous perfusion (washing) of the external surface of the heart led to partial development of the hypodynamic state. However when external perfusion was combined with internal perfusion, the onset of the hypodynamic state was faster reaching a steady-state of around 50% of the original tension after 150 minutes. During this steady state the preparation was used to investigate the inotropic effects of serum, serum fractions and several metabolic substrates including pyruvate, lactate and creatine on the heart. A comparative study was made in order to determine the oxygen consumption and the levels of endogenous lactate, pyruvate and creatine phosphate in the fresh and hypodynamic hearts. The levels of lactate, pyruvate and creatine phosphate were significantly decreased in the hypodynamic hearts comparea with normal preparations. Oxygen consumption was unchanged and contractile force decreased by 47% in the hypodynamic hearts. These initial results show that the development of the weak condition of the heart may be associated with a metabolic deficiency of the myocardium. Perfusion of the isolated spontaneously beating hypodynamic frog heart with dialysed serum taken from several animal species evoked both positive inotropic and chronotropic responses in the presence of cy•adrenergic (phentolamine),/3-adrenergic (propranolol) and cholinergic antagonists (atropine). These effects were dose-dependent. The cardioactive component(s) of serum were separated using several fractionation techniques. These included gel filtration on C50 and C200 Sephadex, filtration on Amicon microconcentrators and ultrafiltration on PM30 and XM100A membranes. During the separation procedures the fractions were tested for inotropic activity compared with dialysed serum. A fraction corresponding to serum albumin in molecular weight (60000-63000) evoked a positive inotropic effect on the heart. Commercial serum albumin evoked no net effect on the heart. Serum and its fractions were subjected to physical and chemical treatments including boiling, pH changes, chymotrypsin and lipase treatment and lipid extraction in an attempt to determine the nature of the cardioactive component(s). During the various stages of treatment the fractions were tested on the heart for bioactivity. Boiling, pH changes and chymotrypsin treatment failed to denature the cardioactive component of serum corresponding to serum albumin in molecular weight. After these treatments a positive inotropic response was still retained. Similar responses were obtained with a lipid extract of serum. However, the activity of these fractions disappeared after treatment with the enzyme lipase suggesting that that the cardioactive component has lipid like properties. No attempt was made to identify and characterise this unknown lipid due to lack of time. In conclusion, the present study demonstrates that serum contains a lipid—like cardioactive fraction which may be associated with serum albumin. It evokes positive inotropic and chronotropic effects on the isolated hypodynamic frog heart.
9
Tory, Rita. "The study of the effect of immunosuppressive drugs on lipid metabolism." Electronic Thesis or Dissertation, University of British Columbia, 2004. http://hdl.handle.net/2429/7593.
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Introduction: Lipid abnormalities including increased total cholesterol, triglycerides, and lowdensity lipoprotein-cholesterol have been frequently reported in renal transplantation and could be involved in the high frequency of cardiovascular disease in this population. Immunosuppressive therapy appears to be a main factor that influences the post-transplant lipid profile. Cyclosporine A (CsA), rapamycin (RAPA), tacrolimus (TAC) and mycophenolate mofetil (MMF) are commonly used immunosuppressant in solid organ transplant patients. Several of these immunosuppressive agents including CsA, RAPA and TAC appear to have a significant effect on patient lipid level. Although RAPA does not seem to cause nephrotoxicity as commonly seen in patients treated with CsA or TAC, it seems to be associated with an incremental increase in triglyceride level. However, the immunosuppressive-induced hyperlipidemia has not been sufficiently described. Purpose: Our aim was to determine the effects of these drugs in vitro on key regulatory enzymes of lipid metabolism; Cholesteryl Ester Transfer Protein (CETP), hepatic lipase (HL) and lipoprotein lipase (LPL) activity within human plasma, as well as the in vivo effects of TAC on these enzymes in renal transplant patients. In addition, we also investigated the effects of RAPA and TAC on cholesterol efflux from human THP-l macrophages. Methods: The effects of CsA, TAC, RAPA and MMF on CETP, HL and LPL activity were first determined in vitro in human normolipidemic plasma and post-heparin normal human plasma, respectively. We further investigated the in vivo effects of TAC on these enzymes activities in renal transplant patients for one month following transplantation. The cholesterol efflux study was conducted independently to assess the effects of RAPA and TAC on ApoA-I- and HDL-mediated cholesterol efflux from human THP-l macrophages, as well as adenosine-triphosphate binding cassette (ABC)Al and ABCG1 protein expressions in these cells. Results: Our in vitro CETP study showed that CsA and RAPA induced CETP activity in human normolipidemic plasma in a dose-dependant manner. Although, none of these drugs, CsA, TAC, RAPA and MMF affected in vitro HL activity, these drugs suppressed the LPL activity in the post-heparin plasma. Unlike TAC, RAPA was shown to decrease apoAl-mediated cholesterol efflux and ABCA1 protein expression in human THP-l macrophages. In agreement with our in vitro result, our clinical study demonstrated that TAC significantly increased triglyceride levels and reduced the LPL activity in the renal transplant patients, regardless of the patients were on statin or not. Conclusions: These findings suggest that the increase in CETP activity, suppression in LPL activity and inhibition in the cholesterol efflux following either CsA, RAPA or TAC treatments observed in the present study may be associated with hypercholesterolemia and hypertriglyceridemia seen in patients administered these drugs.
10
Tory, Rita. "The study of the effect of immunosuppressive drugs on lipid metabolism." Electronic Thesis or Dissertation, University of British Columbia, 2004. http://hdl.handle.net/2429/7593.
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Анотація:
Introduction: Lipid abnormalities including increased total cholesterol, triglycerides, and lowdensity lipoprotein-cholesterol have been frequently reported in renal transplantation and could be involved in the high frequency of cardiovascular disease in this population. Immunosuppressive therapy appears to be a main factor that influences the post-transplant lipid profile. Cyclosporine A (CsA), rapamycin (RAPA), tacrolimus (TAC) and mycophenolate mofetil (MMF) are commonly used immunosuppressant in solid organ transplant patients. Several of these immunosuppressive agents including CsA, RAPA and TAC appear to have a significant effect on patient lipid level. Although RAPA does not seem to cause nephrotoxicity as commonly seen in patients treated with CsA or TAC, it seems to be associated with an incremental increase in triglyceride level. However, the immunosuppressive-induced hyperlipidemia has not been sufficiently described. Purpose: Our aim was to determine the effects of these drugs in vitro on key regulatory enzymes of lipid metabolism; Cholesteryl Ester Transfer Protein (CETP), hepatic lipase (HL) and lipoprotein lipase (LPL) activity within human plasma, as well as the in vivo effects of TAC on these enzymes in renal transplant patients. In addition, we also investigated the effects of RAPA and TAC on cholesterol efflux from human THP-l macrophages. Methods: The effects of CsA, TAC, RAPA and MMF on CETP, HL and LPL activity were first determined in vitro in human normolipidemic plasma and post-heparin normal human plasma, respectively. We further investigated the in vivo effects of TAC on these enzymes activities in renal transplant patients for one month following transplantation. The cholesterol efflux study was conducted independently to assess the effects of RAPA and TAC on ApoA-I- and HDL-mediated cholesterol efflux from human THP-l macrophages, as well as adenosine-triphosphate binding cassette (ABC)Al and ABCG1 protein expressions in these cells. Results: Our in vitro CETP study showed that CsA and RAPA induced CETP activity in human normolipidemic plasma in a dose-dependant manner. Although, none of these drugs, CsA, TAC, RAPA and MMF affected in vitro HL activity, these drugs suppressed the LPL activity in the post-heparin plasma. Unlike TAC, RAPA was shown to decrease apoAl-mediated cholesterol efflux and ABCA1 protein expression in human THP-l macrophages. In agreement with our in vitro result, our clinical study demonstrated that TAC significantly increased triglyceride levels and reduced the LPL activity in the renal transplant patients, regardless of the patients were on statin or not. Conclusions: These findings suggest that the increase in CETP activity, suppression in LPL activity and inhibition in the cholesterol efflux following either CsA, RAPA or TAC treatments observed in the present study may be associated with hypercholesterolemia and hypertriglyceridemia seen in patients administered these drugs.

Книги з теми "Heart Effect of drugs on":

1
Lenson, David. On drugs. Minneapolis: University of Minnesota Press, 1995.
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2
Check, William A. Drugs of the future. New York: Chelsea House, 1987.
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3
Gavin, Katherine T. Investigations of cardiovascular [alpha]-adrenoceptor function. Dublin: University College Dublin, 1997.
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4
Studies, Rutgers Center of Alcohol. Journal of studies on alcohol and drugs. Piscataway, NJ: Alcohol Research Documentation, Inc., Rutgers, the State University of New Jersey, 2007.
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5
Friedman, David P. Drugs and the brain. Bethesda, Md. (9000 Rockville Pike, Bethesda 20892): National Institutes of Health, The Clinical Center, 1993.
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6
Friedman, David P. Drugs and the brain. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1991.
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7
Noble, Denis, and Yung E. Earm, eds. Ionic Channels and Effect of Taurine on the Heart. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3074-9.
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8
Weidensaul, Scott. Mountains of the heart: A natural history of the Appalachians. Golden, Colo: Fulcrum Pub., 1994.
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9
Pang, Catherine C. Y. The effects of drugs on the venous system. Austin: R.G. Landes, 1994.
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10
Buchholz, Garth A. Fastfacts on drugs. [Manitoba]: Awareness & Information Unit of the Addictions Foundation of Manitoba, 1996.
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Статті в газетах з теми "Heart Effect of drugs on":

1
Klid, B. "New Sourcebook of Material on Holodomor." Новий шлях, 14 March 2013.
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2
Gregorovich, A. "Ukrainian Canadians: 200 Years of History - The War of 1812." Новий шлях, 14 June 2012.
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3
Yuzyk, P. "Senator Paul Yuzyk - FA Vision of Diversity Celebrated "Architect of Multiculturalism"." Український голос, 14 August 2017.
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4
Ціон, В. "Як умру, то поховайте my heart in the highlands..." Літературна Україна, 8 лютого 2018.
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5
Плахта, Д. "Glory to Ukraine! Shame on you, FIFA!" День, 11 July 2018.
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6
Gregorovich, A. "Ukrainian Canadians: 200 Years of History - Ukrainians in All Walks of Life." Новий шлях, 13 September 2012.
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7
Manastyrsky, Peter. "Holodomor - Ukrainian Famine of 1932 - 1933." Український голос, 13 November 2017.
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8
Kvit, S. "Fighting for the soul of Ukrainian Education." Церква і життя, 2–22 December 2010.
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9
Тукало, М. ""Єдиний шанс для української науки - Centers of Excellence"". Дзеркало тижня, 12–18 серпня 2017.
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10
Goble, P. "Window on Eurasia: Moscow Moves to Close Ukrainian Institutions in Russia." Гомін України, 8 February 2011.
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Автореферати дисертацій з теми "Heart Effect of drugs on":

1
Андрущенко, Катерина Анатоліївна. "Правова природа концепції "margin of appreciation"". Автореф. дис. канд. юрид. наук, М-во освіти і науки України, Київ. нац. ун-т ім. Тараса Шевченка, 2017.
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2
Стасюк, Б. В. "Часткові еквіваленти у відтворенні англомовних художніх текстів в українському перекладі (на матеріалі романів Дж.Р.Р.Толкіна "The Lord of the Rings" і У.К.Ле Гуїн "A Wizard of Earthsea")". Автореф. дис. канд. філол. наук, КНУТШ, 2011.
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Частини книг з теми "Heart Effect of drugs on":

1
Schwandt, Peter, Markus G. Donner, and Werner O. Richter. "Long-Term Effect of Ldl-Apheresis on Coronary Heart Disease." In Drugs Affecting Lipid Metabolism, 513–19. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_60.
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2
Yang, Charles I., Pravin Taneja, and Peter J. Davis. "Sedative Hypnotic and Anesthetic Agents: Their Effect on the Heart." In Handbook of Pediatric Cardiovascular Drugs, 280–317. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-953-8_12.
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3
Martin, V., A. Drochon, O. Fokapu, and J.-F. Gerbeau. "MagnetoHemoDynamics Effect on Electrocardiograms." In Functional Imaging and Modeling of the Heart, 325–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-21028-0_42.
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4
Bogazzi, Fausto, and Daniele Cappellani. "Heart Drugs and Influences on TH Metabolism." In Thyroid and Heart, 311–25. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36871-5_23.
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5
Manolis, Antonis S., and Antonis A. Manolis. "Effect of Endurance Sport on the Right Heart." In Right Heart Pathology, 157–65. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5_6.
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6
Halberstadt, Adam L., and Mark A. Geyer. "Effect of Hallucinogens on Unconditioned Behavior." In Behavioral Neurobiology of Psychedelic Drugs, 159–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/7854_2016_466.
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7
Simpson, N. B. "The Effect of Drugs on Hair." In Pharmacology of the Skin II, 495–508. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74054-1_37.
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8
Deth, Richard C. "The Effect of Drugs on Attention." In Molecular Origins of Human Attention, 111–24. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0335-4_10.
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9
Nakaya, N., and Y. Goto. "Effect of CS-514 on Hypercholesterolemic Patients." In Drugs Affecting Lipid Metabolism, 274–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_51.
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10
Chatham, John C. "The Effect of Diabetes on Glucose Metabolism." In The Heart in Diabetes, 189–214. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1269-7_9.
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Тези доповідей конференцій з теми "Heart Effect of drugs on":

1
Kazantsev, S. O., and M. S. Korovin. "Nanomaterials potentiating standard chemotherapy drugs’ effect." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS: Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications (PC IPCA’17). Author(s), 2017. http://dx.doi.org/10.1063/1.5001610.
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2
Raugale, A., P. Gaidelis, and A. Januskevicius. "New researches on teratogenic effect of drugs." In SPIE Proceedings, edited by Leonardo Longo, Alfons G. Hofstetter, Mihail-Lucian Pascu, and Wilhelm R. A. Waidelich. SPIE, 2004. http://dx.doi.org/10.1117/12.584335.
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3
De jonckheere, J., M. Jeanne, A. Keribedj, M. Delecroix, and R. Logier. "Closed-loop administration of analgesic drugs based on heart rate variability analysis*." In 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8512330.
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4
Reznikov, Konstantin M., and Pavel D. Kolesnichenko. "THE EFFECT OF DRUGS ON THE THREE-DIMENSIONAL STRUCTURE OF CARDIOMYOCYTES." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.24.
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In experimental myocardial infarction the occurrence of contracture of the sarcomeres, while giperkeratoza adjacent sections of the cell and movement of mitochondria. Drugs (korglikon, procainamide, potassium orotate) have different impacts on these processes.
5
Pashkovsky, Sergey, Darya Gerne, Aleksandra Zenkova, and Valeria Kurochkina. "Effect of Antiviral Drugs on the Phytoseiulus persimilis Ath.-H. Acariphagus." In Proceedings of the International Scientific Conference The Fifth Technological Order: Prospects for the Development and Modernization of the Russian Agro-Industrial Sector (TFTS 2019). Paris, France: Atlantis Press, 2020. http://dx.doi.org/10.2991/assehr.k.200113.214.
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6
Janousek, Oto, Marina Ronzhina, Jakub Hejc, Tibor Stracina, Veronika Olejnickova, Marie Novakova, Ivo Provaznik, and Jana Kolarova. "The Effect of Cardiac Filling on Heart Rate Variability in Rabbit Isolated Heart." In 2016 Computing in Cardiology Conference. Computing in Cardiology, 2016. http://dx.doi.org/10.22489/cinc.2016.143-254.
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7
PRINCI, T., A. ACCARDO, and D. PETEREC. "EFFECT OF BREATHING RATE ON HEART RATE VARIABILITY." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0139.
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8
Ahmad, T. J., H. Ali, S. M. I. Majeed, and S. A. Khan. "Effect of atrioventricular conduction on heart rate variability." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090551.
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9
Xiu-Li Chen and Li-Bing Ma. "The effect of nucleoside anticancer drugs on the development of mouse embryos." In 2011 International Symposium on Information Technology in Medicine and Education (ITME 2011). IEEE, 2011. http://dx.doi.org/10.1109/itime.2011.6130761.
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10
Grigore, Ioana, Laura Mihaela Trandafir, Vasilica Toma, Georgeta Diaconu, Daniela Matei, and Elena Luca. "Effect of anti-epileptic drugs on the oral health of epileptic children." In 2015 E-Health and Bioengineering Conference (EHB). IEEE, 2015. http://dx.doi.org/10.1109/ehb.2015.7391523.
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Звіти організацій з теми "Heart Effect of drugs on":

1
Black, Sandra, Paul Devereux, and Kjell Salvanes. Losing Heart? The Effect of Job Displacement on Health. Cambridge, MA: National Bureau of Economic Research, December 2012. http://dx.doi.org/10.3386/w18660.
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2
Lichtenberg, Frank. The Effect of New Drugs on Mortality from Rare Diseases and HIV. Cambridge, MA: National Bureau of Economic Research, December 2001. http://dx.doi.org/10.3386/w8677.
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3
Crosland, Richard D. Effect of Drugs on the Lethality in Mice of the Venoms and Neurotoxins from Sundry Snakes. Fort Belvoir, VA: Defense Technical Information Center, July 1990. http://dx.doi.org/10.21236/ada228245.
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4
Georgitsis, Micheal. The Effect of Lymph Sac Pressure on Lymph Heart Pressure Development in the Toad Bufo Marinus. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7232.
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5
O'Connor, Kenneth M. Strategic Analysis of the War on Drugs. Fort Belvoir, VA: Defense Technical Information Center, April 1991. http://dx.doi.org/10.21236/ada234230.
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6
Xu, Jian-bo. Effect of grelin on TRX expression in chronic heart failure tissue: a protocol of systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0078.
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7
Lleras-Muney, Adriana, and Frank Lichtenberg. The Effect of Education on Medical Technology Adoption: Are the More Educated More Likely to Use New Drugs. Cambridge, MA: National Bureau of Economic Research, September 2002. http://dx.doi.org/10.3386/w9185.
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8
Brown, Michael. Effect of Ototoxic Drugs on the Amphibian Auditory System: Injection of Gentamicin Sulfate into Anuran Otic Capsules and Recovery of Thresholds. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6734.
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9
Grange, David L. Winning the War on Drugs. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada437503.
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10
Mehegan, Laura, and Laura Skufca. 2015 Survey on Prescription Drugs. AARP Research, April 2016. http://dx.doi.org/10.26419/res.00122.001.
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