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Relevant bibliographies by topics / Drug effects

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Academic literature on the topic 'Drug effects'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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Journal articles on the topic "Drug effects"

1

Bocharova, Inna Anatolevna, Vadim Agadzhanov, and Vadim Sagalaev. "Drug addiction. Drugs and their effects on man." Vestnik Volgogradskogo Gosudarstvennogo Universiteta. Serija 11. Estestvennye nauki, no. 2 (December 1, 2013): 22–27. http://dx.doi.org/10.15688/jvolsu11.2013.2.3.

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Ranasinghe, Leonard, Geetha Amarasinghe, and Amanda Lash. "The Effects of Childhood Trauma on Drug Use." Clinical Medical Reviews and Reports 2, no. 3 (June 22, 2020): 01–07. http://dx.doi.org/10.31579/2690-8794/019.

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Exposure to childhood physical abuse, sexual abuse, emotional abuse, and neglect have been found to have a positive association with drug use. Various studies have demonstrated how individuals may turn to drugs as a form of coping. However, this is a negative form of coping, which can take a toll on one’s mental state and even impact families and society. Studies have reported that a higher number of adverse childhood experiences (ACEs) have a stronger association with substance use later in life [1,3]. Recent research has also demonstrated those who experienced childhood neglect also displayed anxiety or depression, which might suggest a reason for the connection between the negligence and drug use [14]. There is also research that shows that childhood maltreatment could influence one’s susceptibility to drugs and the structural remodeling of the brain [4]. Various types of drugs have been used in association with childhood trauma; however, no single drug was reported to have a greater association than the others. Substance abuse has been a rising issue over the years. With the understanding that childhood trauma could contribute to the onset of drug use, it is essential to gain a better knowledge of the specific types of substance abuse linked to childhood trauma. Future examination of this topic can help raise awareness and educate society on the effects of childhood trauma and how to prevent drug use associated with it.

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Rees, Terry D. "Oral Effects of Drug Abuse." Critical Reviews in Oral Biology & Medicine 3, no. 3 (April 1992): 163–84. http://dx.doi.org/10.1177/10454411920030030101.

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Drug abuse is a major problem in the U.S. and most other countries of the world today. Many studies, surveys, and case reports have described the adverse social and medical effects of drug abuse; yet surprisingly little is known about the specific effects of many of these drugs in the oral cavity. This article reviews the current state of knowledge concerning the systemic and oral effects of drugs of abuse and the dental management of addicted patients.

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Kedyk, Antonina, and Oleksandr Kutsyn. "Metabolic effects of empagliflozine." Diabetes Obesity Metabolic Syndrome, no. 5 (2022): 38–56. http://dx.doi.org/10.57105/2415-7252-2022-5-04.

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Potentially beneficial metabolic effects of empagliflozin remain "overshadowed" by the undeniable benefits of this drug in terms of cardio- and renoprotection. Today, there is a large data array (meta-analyses, systematic reviews and separate cohort studies with empagliflozin) that confirm the beneficial effect of this drug on various metabolic processes, which was systematized in this scientific review. It is emphasized that the antihyperglycemic effect of the drug does not depend on the secretion of insulin by β-cells of the pancreas and insulin resistance, it is manifested only in conditions of glucosuria and limited by eGFR. Empagliflozin combines well with all oral and parenteral hypoglycemic drugs; combination with drugs that have a potential risk of hypoglycemia (insulin and sulfonylurea drugs) requires a dose reduction of the latter. The durability of empagliflozin allows to maintain the achieved levels of glycated hemoglobin for a long time and postpone the start of insulin therapy. Weight loss by drug using corrects blood pressure and insulin resistance. In addition to the ability to reduce the level of uric acid and postpone the appointment of antigout drugs, empagliflozin can be considered a drug that has a multi-vector effect on various component of the metabolic syndrome. Promising areas of the drug using are reducing the risk of nephrolithiasis, steatosis and slowing down the progression of liver fibrosis.

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Halliwell, Barry. "Drug Antioxidant Effects." Drugs 42, no. 4 (October 1991): 569–605. http://dx.doi.org/10.2165/00003495-199142040-00003.

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Terézhalmy, Géza T., and Marsha A. Pyle. "ADVERSE DRUG EFFECTS." Dental Clinics of North America 38, no. 4 (October 1994): 769–83. http://dx.doi.org/10.1016/s0011-8532(22)00189-6.

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Lamy, Peter P. "Adverse Drug Effects." Clinics in Geriatric Medicine 6, no. 2 (May 1990): 293–307. http://dx.doi.org/10.1016/s0749-0690(18)30618-9.

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Goudie, A. J. "Conditioned drug effects." European Journal of Pharmacology 183, no. 1 (July 1990): 98. http://dx.doi.org/10.1016/0014-2999(90)91357-h.

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Larson, Eric B. "Adverse drug effects." Journal of General Internal Medicine 8, no. 6 (June 1993): 342–43. http://dx.doi.org/10.1007/bf02600151.

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Derman, SG, and EY Adashi. "Erratum to: Adverse effects offertility drugs. Drug Saf." Drug Safety 12, no. 3 (March 1995): 208. http://dx.doi.org/10.1007/bf03257466.

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Dissertations / Theses on the topic "Drug effects"

1

Cong, Ze. "Value of pharmaceutical innovation the access effects, diffusion process, and health effects of new drugs /." Santa Monica: RAND, 2009. http://www.rand.org/pubs/rgs_dissertations/2009/RAND_RGSD242.pdf.

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Näsman, Margareta. "Effects of anti-neoplastic therapy on tooth and bone formation : clinical and experimental studies /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3282-4/.

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Gao, Xiang. "Kinetics of drug disposition and effects /." The Ohio State University, 1997. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942739808919.

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Kim, Chang Kwon. "The role of the drug-effect contingency in the development of cross tolerence to anticonvulsant drug effects." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28249.

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It was recently demonstrated that tolerance develops to the anticonvulsant effect of ethanol on kindled convulsions elicited in rats by electrical stimulation of the amygdala, following each of a series of ethanol injections delivered on a bidaily schedule (once every 48 hr). The tolerance developed only when the convulsive stimulation was administered during the periods of ethanol exposure: subjects that received ethanol 1.5 hr before each convulsive stimulation demonstrated tolerance after just five ethanol injections; whereas, no tolerance was evident in subjects that received ethanol 1.5 hr after each stimulation. Such tolerance, which is not the inevitable product of drug exposure but is contingent upon the expression of the drug effect--the anticonvulsant effect in this case--has been termed contingent tolerance. In Experiment 1A, tolerance developed to the anticonvulsant effects of bidaily IP injections of phenobarbital (30 mg/kg), trimethadione (270 mg/kg) and clonazepam (0.40 or 0.35 mg/kg) delivered 1 hr before each convulsive stimulation. In Experiment IB, the rats tolerant to the anticonvulsant effects of phenobarbital, trimethadione, or clonazepam received bidaily injections of carbamazepine (35 mg/kg, IP), administered 1 hr before each stimulation. There was a statistically significant transfer of tolerance from phenobarbital to carbamazepine, but not from either trimethadione or clonazepam to carbamazepine. Thus, cross tolerance appears to be greatest between anticonvulsant drugs that are effective against a similar profile of clinical and experimental seizures and that have similar mechanisms of action. In Experiment 2A, tolerance developed to the anticonvulsant effect of bidaily pentobarbital (15 mg/kg, IP) injections only in those rats that received the drug 1 hr before the convulsive stimulation, but not in those rats that had received the drug 1 hr after each stimulation. Furthermore, those rats that had received the convulsive stimulations while under the influence of pentobarbital subsequently displayed a greater degree of cross tolerance to the anticonvulsant effect of ethanol (1.5 g/kg, IP) than those that had received the drug after each stimulation (contingent cross tolerance). Experiment 2B was the converse of Experiment 2A: contingent tolerance was demonstrated to ethanol and contingent cross tolerance to pentobarbital. This study provided the first unambiguous and bidirectional demonstration that the drug-effect contingency plays an important role in the development of cross tolerance. In Experiment 3, tolerance to the anticonvulsant effect of ethanol dissipated when bidaily pentobarbital (15 mg/kg, IP) injections were delivered 1 hr after each convulsive stimulation (contingent cross-dissipation of tolerance), but did not dissipate when it was delivered 1 hr before each stimulation. Thus, the drug-effect contingency was shown to be important in the dissipation of tolerance to one drug following the administration of another drug. In Experiment 4, different groups of rats received different doses of pentobarbital (10-50 mg/kg, IP) on a bidaily schedule 1 hr before the convulsive stimulation. Greater tolerance was found to the anticonvulsant effect of pentobarbital in rats that had received successively larger doses of the drug, none of which were large enough to suppress the convulsions, than those rats that were maintained on a high dose of the drug that completely suppressed the convulsions. The greater tolerance in the group that received successively greater doses was attributed to the fact that the convulsions were experienced in the drugged state. This study challenged the generally accepted view that tolerance develops more rapidly and to a greater extent with larger drug doses . This thesis provides the first unambiguous and systematic evidence of the role of the drug-effect contingency in the transfer of tolerance from one drug to another, and in the dissipation of tolerance to one drug following the administration of another. On the basis of the present experiments, several elaborations were proposed to the drug-effect theory of drug tolerance, which claims that tolerance develops to drug effects and not to drug exposure per se.
Arts, Faculty of
Psychology, Department of
Graduate

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Feeney, Thomas P. "Effects of drug dependence on matrimonial consent." Online full text .pdf document, available to Fuller patrons only, 2003. http://www.tren.com.

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Lau, Phyllis Min-yu. "Adverse drug reactions in oncology." Monash University, Dept. of Pharmacy Practice, 2003. http://arrow.monash.edu.au/hdl/1959.1/5549.

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Hasegawa, Takaaki, Kenji Takagi, and Kiyoyuki Kitaichi. "Effects of Bacterial Endotoxin on Drug Pharmacokinetics." 名古屋大学医学部, 1999. http://hdl.handle.net/2237/6203.

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Buggins, Talia Rae. "Effects of pharmaceutical excipients on drug disposition." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55658/.

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This thesis investigates the potential of some commonly used pharmaceutical excipients to alter drug pharmacokinetics. In breath test studies, 3.2ml/kg DMSO prolonged the half-life of 14C-aminopyrine, -erythromycin and -NDMA, indicating in vivo inhibition of metabolism by CYP3A (erythromycin), CYP2E1 (NDMA) and the variety of enzymes that metabolise aminopyrine (CYP 2C11, 2C12, 2B1 and 2B2). However, no effects were apparent at doses typically used in pre-clinical formulations. Aminopyrine and erythromycin breath tests were not affected by propylene glycol (PG) or Solutol HS15, however PG did significantly increase 14C02 exhalation half- life in the NDMA breath test, suggesting a specific effect on metabolism by CYP2E1. While two 2ml/kg doses of DMSO increased plasma ai-AGP levels, none of the excipients tested consistently affected plasma ai-AGP at doses commonly used in pre-clinical formulations, suggesting that they are unlikely to increase protein binding by this mechanism. Transport studies in MDCK-MDR1 cells demonstrated an inhibitory effect of 0.1% Tween 80 and Solutol HS15 on P-Gp. In vivo, Tween inhibited the biliary elimination of 99mTc-MIBI but not 99mTc-HIDA, indicating inhibition of P-Gp, while Solutol inhibited the biliary elimination of both radiopharmaceuticals, suggesting inhibition of MRP and possibly P-Gp. Pre-treatment with 4ml/kg DMSO substantially impaired the renal elimination of 99mTc-DTPA. In contrast, 20% 1.8ml/kg DMSO significantly increased 99mTc-DTPA uptake into the kidneys, suggesting an increase in GFR. Both Tween and Solutol delayed 99mTc-DTPA elimination from the kidneys in some rats, without affecting GFR. However, Solutol did not significantly affect the pharmacokinetics of OAT or OCT substrates, suggesting it did not affect active renal secretion by these transporters. These results demonstrate that excipients can influence drug pharmacokinetics in vivo, after a single acute dose at levels commonly used in pre clinical studies.

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Bradshaw, Jennifer Jean. "Isoflurane : interaction with hepatic microsomal enzymes." Doctoral thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27138.

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lsoflurane interacts with cytochrome P-450 in rat and human hepatic microsomes and the Δ6- and Δ5-desaturases in rat hepatic microsomes. The interaction of isoflurane with cytochrome P-450 results in its metabolism to fluoride ion and organofluorine metabolites. The cytochrome P-450 isozymes catalysing the defluorination of isoflurane were assessed in hepatic microsomes from phenobarbital-, β-naphthoflavone- and pregnenolone-16α-carbonitrilepretreated and untreated rats. One or more of the cytochrome P-450 isozymes induced by phenobarbital and pregnenolone-16α-carbonitrile appear to defluorinate isoflurane, but those induced by β-naphthoflavone do not. From a comparison of the extent of defluorination of isoflurane in hepatic microsomes from phenobarbital- and pregnenolone-16α-carbonitrile-pretreated rats, and their Kₘ and Vₘₐₓ values, it appears that isoflurane is defluorinated by one or more isozymes induced by both phenobarbital and pregnenolone-16α-carbonitrile. The major isozyme is probably cytochrome P-450PCN1. The metabolites of isoflurane were identified in human and phenobarbital-induced rat hepatic microsomes. In microsomes from phenobarbital-pretreated rats, isoflurane is metabolised to fluoride ion and trifluoroacetaldehyde; trifluoroacetic acid is not produced in measureable amounts. The trifluoroacetaldehyde produced binds to microsomal constituents. In human hepatic microsomes, the organofluorine metabolite is identified as trifluoroacetic acid. It is proposed that isoflurane is metabolised by different pathways in human and phenobarbital-induced rat hepatic microsomes. The interaction of isoflurane with the cyanide-sensitive factors was assessed by several criteria. Firstly, using the reoxidation of cytochrome b₅ as an index of fatty acid desaturase activity, isoflurane appears to interact with the Δ6- and/or Δ5-desaturases, but not the Δ9-desaturase. Secondly, these results were confirmed and clarified by the use of direct assays to measure the fatty acid desaturase activity. Using the direct assay, we confirmed that isoflurane did not inhibit the Δ9-desaturase and inhibited Δ6-desaturation of linoleic acid, but not the Δ6-desaturation of α-linolenic acid. The inhibition of the Δ6-desaturation of linoleic acid occurred at low millimolar concentrations of isoflurane. lsoflurane inhibits the Δ5-desaturation of eicosa-8, 11, 14-trienoic acid to a small extent which is only apparent at much higher concentrations of isoflurane than that which inhibits the Δ6-desaturase. Further studies focussed on measurement of the activity of Δ6-desaturase in order to attempt to study the kinetics of the inhibition of the Δ6-desaturase by isoflurane: Δ6-desaturase activity was assessed using hepatic microsomes as the source of the enzyme and linoleic acid as substrate precursor. In the course of these studies, we identified a number of factors that affected the apparent activity of the Δ6-desaturase in hepatic microsomes. These included significant levels of endogenous substrate and competing reactions in the hepatic microsomes. Endogenous substrate levels were quantified and corrected for. We then resorted to computer modelling to extract the kinetics of the Δ6-desaturase free of contributions from acyl-CoA synthetase and lysophospholipid acyltransferase, as well as enzyme decay. The kinetics of isoflurane inhibition of the Δ6-desaturase were then superimposed and studied by computer modelling.

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Sangfelt, Olle. "Effects of interferon on cellular proliferation and apoptosis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19981014sang.

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Books on the topic "Drug effects"

1

Kelly, Jennifer C. Adverse Drug Effects. New York: John Wiley & Sons, Ltd., 2006.

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Stephens, M. D. B. The detection of new adverse drug reactions. 2nd ed. London: Macmillan Press ; New York, NY : Stockton Press, 1988.

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Fraunfelder, Frederick T. Drug-induced ocular side effects. Edited by Randall Joan A. 4th ed. Baltimore: Williams & Wilkins, 1996.

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Liu, Xiaodong, and Guoyu Pan, eds. Drug Transporters in Drug Disposition, Effects and Toxicity. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7647-4.

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Martha, Meyer S., ed. Drug-induced ocular side effects and drug interactions. 3rd ed. Philadelphia: Lea & Febiger, 1989.

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A, Routledge P., and Talbot J. C. C, eds. Detection of new adverse drug reactions. 4th ed. London: Macmillan Reference Ltd, 1998.

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Uetrecht, Jack P. Adverse drug reactions. Heidelberg: Springer, 2010.

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Dukes, Graham. The Effects of Drug Regulation. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-011-7327-8.

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Baselt, Randall C. Drug effects on psychomotor performance. Foster City, Calif: Biomedical Publications, 2001.

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C, Talbot J. C., ed. The detection of new adverse drug reactions. New York, N.Y: Stockton Press, 1985.

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Book chapters on the topic "Drug effects"

1

Simola, Nicola, Micaela Morelli, Tooru Mizuno, Suzanne H. Mitchell, Harriet de Wit, H. Valerie Curran, Celia J. A. Morgan, et al. "Drug Effects." In Encyclopedia of Psychopharmacology, 431. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3206.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "Aversive Drug Effects." In Encyclopedia of Psychopharmacology, 192. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3088.

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Gualtieri, C. Thomas. "Inadvertent Drug Effects." In Neuropsychiatry and Behavioral Pharmacology, 89–101. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4613-9036-7_4.

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Banasikowski, Tomek J., and Richard J. Beninger. "Conditioned Drug Effects." In Encyclopedia of Psychopharmacology, 410–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-36172-2_145.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Conditioned Drug Effects." In Encyclopedia of Psychopharmacology, 325–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_145.

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Stewart, Jane, and Roelof Eikelboom. "Conditioned Drug Effects." In Handbook of Psychopharmacology, 1–57. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1819-4_1.

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Banasikowski, Tomek J., and Richard J. Beninger. "Conditioned Drug Effects." In Encyclopedia of Psychopharmacology, 1–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27772-6_145-2.

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Pichler, Werner J., and Paolo Campi. "Adverse Side Effects to Biological Agents." In Drug Hypersensitivity, 151–65. Basel: KARGER, 2007. http://dx.doi.org/10.1159/000104198.

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de Kuijper, Gerda M., Arne Risselada, and Rianne van Dijken. "Monitoring Drug Side-Effects." In Handbook of Intellectual Disabilities, 275–301. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20843-1_17.

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Hoyer, Daniel, Eric P. Zorrilla, Pietro Cottone, Sarah Parylak, Micaela Morelli, Nicola Simola, Nicola Simola, et al. "Context-Specific Drug Effects." In Encyclopedia of Psychopharmacology, 350. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3169.

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Conference papers on the topic "Drug effects"

1

Zarandi, Marjan Molavi, Rosaire Mongrain, and Olivier F. Bertrand. "Modeling Drug Eluting Stents for Coronary Artery Bifurcation Considering Non-Newtonian Effects." In ASME 2010 3rd Joint US-European Fluids Engineering Summer Meeting collocated with 8th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2010. http://dx.doi.org/10.1115/fedsm-icnmm2010-31190.

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Drug Eluting Stents (DES) are commonly used for the treatment of stenotic arteries. Restenosis can be treated by delivering anti-thrombotic and anti-proliferative drugs to the arterial wall. The main mechanism of the drug eluting stent is to allow diffusion of the drug from the coating on the stent, into the arterial wall over a prolonged period of time. Investigation of blood flow hemodynamics and shear stress are of great importance in understanding the transport of drugs through the circulatory systems and predicting the performance of drug eluting stents. While drug eluting stent effectively reduces restenosis rate, the conventional drug eluting stent should be optimized to be used in the bifurcation stenting. Various flow patterns due to specific designs of drug eluting stent influence drug delivery. Numerical simulation techniques are appropriate approaches to study such phenomena which can be used to optimize the design of drug eluting stents for bifurcations. In this paper, the complexity of drug eluting stent function in the bifurcation is presented by employing computational fluid dynamics analysis for various stent strut designs. Drug transportation through the lumen and determination of local drug concentrations in arterial wall is carried out for both Newtonian and non-Newtonian flow conditions. It is, to the author’s best knowledge, the first investigation of drug dispersion in arterial bifurcation considering the effects of both the blood rheological properties and stent strut design.

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Tang, Jack C., Jenny T. Mac, Raviraj Vankayala, Allen Partono, Wangcun Jia, and Bahman Anvari. "Effects of Freezing on Erythrocyte-derived Optical Nanoprobes." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/omp.2017.omtu2d.4.

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Cheburkanov, Vsevolod, Junwei Du, David M. Brogan, Mikhail Y. Berezin, and Vladislav V. Yakovlev. "Investigating chemotherapy effects on peripheral nerve elasticity." In Visualizing and Quantifying Drug Distribution in Tissue VIII, edited by Conor L. Evans and Kin Foong Chan. SPIE, 2024. http://dx.doi.org/10.1117/12.3003568.

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Welch, Tre R., Robert C. Eberhart, and Cheng-Jen Chuong. "Thermal Treatment Effects Upon the Degradation Characteristics of PLLA Coiled Stents." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206884.

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Stents are a medical device used to restore blood flow in stenosed vessels. During the process of stent expansion, the balloon and stent could damage the endothelial lining of the vascular wall and alter the mechanical stress states of various tissue components. The evolution of stents has progressed from bare metal stents to drug eluting stents or stents coated with drugs such as Sirolimus. Drug eluting stents are currently used to address the restenosis event that occurs after implantation. These stents have been effective but late stent thrombosis has been an emerging issue with drug eluting stents. Bioresorbable stents have emerged as a potential candidate for drug eluting stents. Su 03 has shown drug-loading PLLA with curcumin can be used as an anti-inflammatory agent. We have developed an internally coiled, furled helical PLLA fiber stent at our institution [Su 03, Zilberman 02, 04, 05]. We have previously shown the effect of 62°C thermal annealing on the expansive characteristics of this stent [Welch 08].

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Dammann, Marc, Christine Mahlke, and Manfred D. Kessler. "Imaging of drug effects in perfused liver." In International Symposium on Biomedical Optics, edited by Manfred D. Kessler and Gerhard J. Mueller. SPIE, 2002. http://dx.doi.org/10.1117/12.469470.

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Bumsoo Han and Ka Yaw Teo. "Effects of freezing on intratumoral drug transport." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5333804.

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Oliveira, Eduardo Felipe da Silva, and Dário César de Oliveira Conceição. "Magnetic drug-carrying nanoparticles in cancer treatments." In II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-074.

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Abstract Magnetic nanoparticles are nanomaterials that are magnetically influenced by an external gradient. The engineering and manipulation of matter at the molecular level presents several advantages in the field of nanomedicine since most biological molecules exist and function at the nanoscale. Magnetic nanoparticles are promising methods for targeted drug delivery that allow for spatially, temporally and dosage-tunable drug release with minimal side effects. The most commonly used magnetic nanoparticles are Magnetite (Fe3O4) and Maghemite (Fe2O3). The function of drug carriers, or "Drugs delivery" is to take the drug to the pharmacological target, reducing the side effects observed in the drugs, also reducing the amount of drug administered, thus obtaining the pharmacological treatment in an optimized way. This study aims to analyze the use of drug-loading magnetic nanoparticles in cancer treatments.

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Chen, Yu, Hui-Fang Cui, Jian-Shan Ye, Ser-Choong Chong, Tit-Meng Lim, Fwu-Shan Sheu, and Hui-Wing Cheong. "Microelectrodes integrated cell-chip for drug effects study." In MOEMS-MEMS 2006 Micro and Nanofabrication, edited by Ian Papautsky and Wanjun Wang. SPIE, 2006. http://dx.doi.org/10.1117/12.647091.

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Naran, P., A. Sharma, E. Scullion, C. Chen, S. Tiberi, V. White, H. Kunst, and E. Skyllberg. "P139 Adverse effects of drugs used in the treatment of multi-drug resistant tuberculosis." In British Thoracic Society Winter Meeting 2023, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 22 to 24 November 2023, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2023. http://dx.doi.org/10.1136/thorax-2023-btsabstracts.290.

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Chen, Peng, Jian Wang, Hongfei Lin, Yichen Wang, Di Zhao, and Yijia Zhang. "Syntactic Type-aware Graph Attention Network for Drug-drug Interactions and their Adverse Effects Extraction." In 2022 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2022. http://dx.doi.org/10.1109/bibm55620.2022.9995045.

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Reports on the topic "Drug effects"

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Ciapponi, Agustín. What are the effects of reference pricing and other pharmaceutical pricing and purchasing policies? SUPPORT, 2016. http://dx.doi.org/10.30846/1608143.

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Pharmaceutical pricing and purchasing policies are used to determine or affect the prices that are paid for drugs. This review found evidence for reference pricing, index pricing, and maximum prices. In reference pricing a reference drug is chosen amongst identical or similar medicines or therapeutically equivalent and the price of the reference drug is reimbursed for all the drugs in that group of drugs. For drugs that are more expensive than the reference drug, the patient has to pay the cost above the reference price. An index price is the maximum refundable price to pharmacies for drugs within an index group of therapeutically interchangeable drugs. A maximum price is a fixed price that attempts to secure pharmaceutical prices that are considered ‘reasonable’ for a given health system.

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Cawley, John, and John Rizzo. The Competitive Effects of Drug Withdrawals. Cambridge, MA: National Bureau of Economic Research, March 2005. http://dx.doi.org/10.3386/w11223.

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Lakdawalla, Darius, and Neeraj Sood. The Welfare Effects of Public Drug Insurance. Cambridge, MA: National Bureau of Economic Research, October 2007. http://dx.doi.org/10.3386/w13501.

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Kaplan, Gary B. Fear Conditioning Effects on Sensitivity to Drug Reward. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada538749.

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Kaplan, Gary. Fear Conditioning Effects on Sensitivity to Drug Reward. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada547601.

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Pearce, Oliver, and Mohga Kamal-Yanni. Harmful Side Effects: How drug companies undermine global health. Oxfam GB, September 2018. http://dx.doi.org/10.21201/2018.3217.

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Karami, Ali, Hamid Tebyanian, Aref Barkhordari, Ebrahim Motavallian, Reza Sayyad Soufdoost, and Mohammad Reza Nourani. Healing Effects of Ointment Drug on Full-thickness Wound. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2019. http://dx.doi.org/10.7546/crabs.2019.01.16.

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Gertner, Jeffrey W., Christopher A. Duplessis, Linda M. Hughes, David M. Fothergill, and Derek Schwaller. Evaluation of Drug Effects on Eustachian Tube Dysfunction in Divers. Fort Belvoir, VA: Defense Technical Information Center, February 2010. http://dx.doi.org/10.21236/ada514519.

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Wozniak, Abigail. Discrimination and the Effects of Drug Testing on Black Employment. W.E. Upjohn Institute, June 2012. http://dx.doi.org/10.17848/wp13-195.

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Ketcham, Jonathan, and Kosali Simon. Medicare Part D's Effects on Elderly Drug Costs and Utilization. Cambridge, MA: National Bureau of Economic Research, September 2008. http://dx.doi.org/10.3386/w14326.

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