Relevant bibliographies by topics / Therapeutics, pharmacological

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Therapeutics, pharmacological'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 January 2023

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Journal articles on the topic "Therapeutics, pharmacological"

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Kim, Doyoung, and Sujin Park. "Pharmacological therapeutics in androgenetic alopecia." Journal of the Korean Medical Association 63, no. 5 (May 10, 2020): 277–85. http://dx.doi.org/10.5124/jkma.2020.63.5.277.

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Androgenetic alopecia (AGA) is the most common type of hair loss and affects both men and women. Male pattern hair loss shows characteristic frontal recession and vertex baldness, whereas female pattern hair loss produces diffuse alopecia over the mid-frontal scalp. AGA is mediated by increased androgen susceptibility in affected scalp hairs. 5α-Reductase converts testosterone into dihydrotestosterone, a potent androgen, in the scalp. Both androgen receptors and 5α-reductase have higher expression levels in the balding scalp than in non-affected regions. Increased androgen susceptibility induces hair follicle miniaturization, which leads to the progressive loss of thicker terminal hairs in the balding scalp. Currently, topical minoxidil and oral 5α-reductase inhibitors, such as finasteride and dutasteride, are approved options for the pharmacological treatment of AGA. Topical minoxidil remains the mainstay of therapy for mild to moderate AGA in both men and women. The daily intake of 1-mg finasteride or 0.5-mg dutasteride shows better efficacy than topical minoxidil in regard to hair regrowth in male AGA. Anti-androgens can be used in female AGA wit clinical and biochemical evidence of hyperandrogenism. Patients may be overwhelmed and confused by the variety of treatment options for AGA management, including over-the-count drugs with low evidence quality. Therefore, physicians must be aware of the current guidelines for the management of AGA based on evidence-based approaches to select better options for patients.
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McMahon, F. Gilbert. "The Pharmacological Basis of Therapeutics." American Journal of Tropical Medicine and Hygiene 35, no. 3 (May 1, 1986): 673. http://dx.doi.org/10.4269/ajtmh.1986.35.673.

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Davies, J. E. "The pharmacological basis of therapeutics." Occupational and Environmental Medicine 64, no. 8 (August 1, 2007): e2-e2. http://dx.doi.org/10.1136/oem.2007.033902.

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Elovic, Elie. "Pharmacological Therapeutics in Nutritional Management." Journal of Head Trauma Rehabilitation 15, no. 3 (June 2000): 962–64. http://dx.doi.org/10.1097/00001199-200006000-00009.

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Woog, J. J. "The Pharmacological Basis of Therapeutics." Archives of Ophthalmology 104, no. 3 (March 1, 1986): 342–43. http://dx.doi.org/10.1001/archopht.1986.01050150036019.

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Papageorgiou, Maria, and Emmanuel Biver. "Interactions of the microbiome with pharmacological and non-pharmacological approaches for the management of ageing-related musculoskeletal diseases." Therapeutic Advances in Musculoskeletal Disease 13 (January 2021): 1759720X2110090. http://dx.doi.org/10.1177/1759720x211009018.

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Despite major progress in the understanding of the pathophysiology and therapeutic options for common ageing-related musculoskeletal conditions (i.e. osteoporosis and associated fractures, sarcopenia and osteoarthritis), there is still a considerable proportion of patients who respond sub optimally to available treatments or experience adverse effects. Emerging microbiome research suggests that perturbations in microbial composition, functional and metabolic capacity (i.e. dysbiosis) are associated with intestinal and extra-intestinal disorders including musculoskeletal diseases. Besides its contributions to disease pathogenesis, the role of the microbiome is further extended to shaping individuals’ responses to disease therapeutics (i.e. pharmacomicrobiomics). In this review, we focus on the reciprocal interactions between the microbiome and therapeutics for osteoporosis, sarcopenia and osteoarthritis. Specifically, we identify the effects of therapeutics on microbiome’s configurations, functions and metabolic output, intestinal integrity and immune function, but also the effects of the microbiome on the metabolism of these therapeutics, which in turn, may influence their bioavailability, efficacy and side-effect profile contributing to variable treatment responses in clinical practice. We further discuss emerging strategies for microbiota manipulation as preventive or therapeutic (alone or complementary to available treatments) approaches for improving outcomes of musculoskeletal health and disease.
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Lee, Chris W., Arulmani Manavalan, and Dana Clausen. "Pharmacological chaperone therapeutics for Krabbe disease." Molecular Genetics and Metabolism 126, no. 2 (February 2019): S92. http://dx.doi.org/10.1016/j.ymgme.2018.12.229.

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Virgen, Celina G., Neil Kelkar, Aaron Tran, Christina M. Rosa, Diana Cruz-Topete, Shripa Amatya, Elyse M. Cornett, Ivan Urits, Omar Viswanath, and Alan David Kaye. "Pharmacological management of cancer pain: Novel therapeutics." Biomedicine & Pharmacotherapy 156 (December 2022): 113871. http://dx.doi.org/10.1016/j.biopha.2022.113871.

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Maynard, R. L. "The Pharmacological Basis of Therapeutics. 9th ed." Occupational and Environmental Medicine 54, no. 1 (January 1, 1997): 69. http://dx.doi.org/10.1136/oem.54.1.69.

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Ikegaya, Yuji, and Eiichi Hinoi. "Toward a New Era of Pharmacological Therapeutics." YAKUGAKU ZASSHI 133, no. 12 (December 1, 2013): 1335–36. http://dx.doi.org/10.1248/yakushi.13-00228-f.

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Dissertations / Theses on the topic "Therapeutics, pharmacological"

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Kay, Katherine. "Pharmacological modelling to investigate antimalarial drug treatment." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/12413/.

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Malaria remains a major public health concern for billions of people worldwide. Achieving the ambitious goal of malaria eradication requires co-ordination of control strategies dealing with a range of parasite, vector, human, social and environmental factors. Availability of effective antimalarial treatment is a key component in malaria control. However the number of drugs available is limited and drug resistance, particularly in Plasmodium falciparum, has now been reported for all currently available antimalarials. Mathematical models provide the opportunity to explore key features underlying antimalarial drug action, effectiveness and resistance. They further allow investigation into questions that cannot otherwise be easily addressed, either because they are too expensive, unethical or logistically too complex. This thesis aims to develop pharmacological models to investigate antimalarial drug treatment. In Chapter 2 we develop a pharmacokinetic-pharmacodynamic (PK/PD) model of antimalarial drug treatment (calibrated using published data) and use it to investigate the efficacy of artemisinin combination therapies (ACTs). Chapter 3 addresses two assumptions built into the methodology that limit the models future application. The model now allows for (i) time lags and drug concentration profiles for drugs absorbed across the gut wall and, if necessary, converted to another active form (ii) multiple drugs within a treatment regimen (iii) differing modes of drug action in combinations (iv) modelling drugs converted to an active metabolite with similar modes of action. In Chapter 4 we extend the methodology to allow for i) the presence of more than one clone when treatment begins (ii) the acquisition of new clones during treatment follow-up (iii) the tracking of individual clones using molecular markers. We then use these extensions to simulate clinical trial data to determine the best methods of analysis. Chapter 5 details how the drug action components of the extended PK/PD model were incorporated into OpenMalaria; a mathematical model of malaria epidemiology allowing investigation of the effects of various intervention strategies including malaria vaccines, vector control strategies and antimalarial drug treatment. In Chapter 6 we investigate the ability of clinical trials to accurately estimate (WoS) using the extended PK/PD model. Windows of selection (WoS) are often used to quantify the genetic process whereby parasites evolve increasing tolerance to antimalarial drugs. We noted a conspicuous lack of comprehensive, good-quality PK datasets currently available in the literature. Despite this, the models produced results highly consistent with field data. They were applied to investigate the potential implications of drug resistance and to make predications about the future effectiveness of antimalarials. We emphasise the value of mathematical models by simulating ‘field data’ to assess the best methods of analysing clinical trials and to investigate the predictive ability of WoS. While we do not suggest models can replace the information gained in clinical trials, this work does demonstrate the importance of mathematical models capable of generating results consistent with field data.
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Hoffman, Benjamin. "The Genetics of Cancer in Pharmacological Drug Development." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/212455.

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Molecular and Cellular Physiology
Ph.D.
The field of cancer therapeutic development has been dominated by two research and discovery paradigms, the cytotoxicity-based or phenotype driven strategy and the target-based rational approach. This thesis describes the standardization of novel assays used in both approaches and the discoveries made using these processes. Rational drug design or the target-based approach to discovering novel anti-cancer agents requires a basic understanding of the oncogenic signals that induce uncontrolled cellular proliferation. c-MET is a proto-oncogene, linked to a number of different cancers, that encodes a receptor tyrosine kinase. As an oncogene, c-MET has been shown to transform cells in the laboratory setting and is dysregulated in number of malignancies. Thus, we sought to discover a small molecule inhibitor of c-MET kinase activity by screening a novel library of small molecules. In the second part of this dissertation, we describe the standardization of a high-throughput assay to identify putative c-MET inhibitors and the results of our screening attempt. Cytotoxicity-based screening is another validated approach that is used to discover anti-cancer agents. As a parallel program to our c-MET discovery effort, we designed a high-throughput cytotoxicity assay to identify a novel small molecule with high cytotoxic activity towards tumor cells. The result of this screen was the identification of ON015640, a novel anti-cancer therapeutic with tubulin-depolymerizing activity. Throughout the course of this project, we tried to discern the advantages and disadvantages of the two predominant paradigms in cancer therapeutic research. Both strategies require careful assay design and an acute understanding of the molecular and genetic underpinnings of cancer. While it is clear that structure-based rational drug design has its merits and its success stories, it has become increasingly clear that seeking out a desired biological effect may serve as a more effective staring point when dealing with cancers for which no clear oncogene addiction phenotype has been observed.
Temple University--Theses
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Shelton, Luke. "The physiological, pharmacological and toxicological roles of Nrf2 in the kidney." Thesis, University of Liverpool, 2015. http://livrepository.liverpool.ac.uk/2014505/.

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Nrf2 is a transcription factor that, under conditions of chemical stress, is able to evade its cytosolic repression and translocate to the nucleus to initiate the transcription of a battery of cytoprotective genes, such as those involved in the detoxication of xenobiotics. Nrf2 has previously been shown to afford protection against chronic and acute renal injury, yet, relatively little is known about the mechanism by which Nrf2 affords this protection, and the extent of its transcriptional roles in the kidney. This thesis seeks to further our understanding of the physiological, pharmacological and toxicological roles of Nrf2 in the kidney. Using an iTRAQ-based proteomic approach to quantify protein expression levels in the kidneys of Nrf2+/+ and Nrf2-/- mice, acutely treated with vehicle or the potent Nrf2 inducer CDDO-Me (3 mg/kg), we demonstrated that 189 proteins were differentially expressed in the Nrf2-/- mouse kidney, compared to Nrf2+/+, and 42 proteins were differentially expressed in the CDDO-Me treated Nrf2+/+ mouse kidney, compared to vehicle. The key finding was that the kidneys of Nrf2-/- mice are deficient in proteins that mediate cellular redox balance, the metabolism of a range of xenobiotics, and the regulation of core metabolic processes, including energy metabolism and the synthesis and recycling of amino acids. Functional demonstration of a reduction in energy metabolism was demonstrated by assessing total NADPH and GSH, of which Nrf2-/- mouse kidneys had 35% and 30% less than their Nrf2+/+ counterparts, respectively. A single acute dose of CDDO-Me failed to augment the expression of proteins, other than Nqo1, that were shown to be regulated by Nrf2 at the basal level in the mouse kidney, however qPCR analysis of these kidneys revealed that CDDO-Me has an effect at the transcriptional level which has not fully translated within the timeframe of this study. In summary, we have provided evidence that Nrf2 regulates the expression of an array of proteins that contribute to cell defence and the maintenance of homeostasis in the kidney, supporting current interest in Nrf2 as a novel therapeutic target in a number of renal diseases. MicroRNAs are a recently discovered RNA-regulatory element that show promise in their use as biomarkers of physiological and pathological events. In order to provide insight into the microRNAs under Nrf2 control in the kidney, we performed an unbiased microRNA array analysis on kidney homogenates from Nrf2+/+ and Nrf2-/- mice, treated with vehicle or CDDO-Me, and then validated several promising microRNA candidates using targeted qPCR analysis. Of particular note are miR-466h-3p, the expression of which was significantly increased in the CDDO-Me treated Nrf2+/+ mouse kidney and decreased in the Nrf2-/- mouse kidney, compared to their respective controls, and miR-28c and 144, which were both significantly decreased in the CDDO-Me treated Nrf2+/+ mouse kidney, and increased in the Nrf2-/- mouse kidney. This novel analysis represents the first step in characterising the renal Nrf2 microRNA-ome, which could reveal novel mechanisms of Nrf2 function and markers of its activity that could translate to the clinic. Recent interest in the use of CDDO-Me as a therapeutic intervention for late-stage chronic kidney disease has culminated in a phase III clinical trial (BEACON), which was subsequently terminated due to unforeseen adverse cardiac events, of which the cause has yet to be identified. In order to determine whether the drive to produce more potent Nrf2 inducers has inadvertently led to the generation of inherently more toxic compounds, the relationship between potency towards Nrf2 and toxicity was evaluated for CDDO-Me and related triterpenoids, and other classes of Nrf2 inducer. Using a rat H4IIE-ARE8L luciferase reporter cell line to determine in vitro therapeutic indices, it was discovered that within the compounds tested an increase in potency toward Nrf2 of four magnitudes results was associated with an increase in toxicity of only two magnitudes, resulting in a relative increase in in vitro safety. This data indicates that it is possible to generate potent Nrf2-inducers that are not inherently toxic, and suggests that therapeutic targeting of Nrf2 continues to hold promise as a novel treatment for a range of diseases. In summary, by using a proteomic approach we have identified an array of renal Nrf2-regulated proteins that contribute to various cytoprotective and metabolic processes in the kidney, supporting current interest in the therapeutic targeting of Nrf2 as treatment for renal disease. Additionally, the microRNAs under Nrf2 regulation in the kidney have also been identified, and represent the first step in fully characterising the Nrf2 microRNA-ome. Finally, it was shown that the drive to produce more potent Nrf2 inducers has not led to the generation of inherently more toxic compounds; indeed an increase in potency is associated with a relative increase in in vitro safety, suggesting that the targeting of Nrf2 is still a promising therapeutic route. Overall, the work presented in this thesis has furthered our understanding of the physiological, pharmacological and toxicological roles of Nrf2 in the kidney.
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Kareem, Hamad B. "Molecular pharmacological studies of CHFI-FXII interaction and FXII function." Thesis, University of Nottingham, 2016. http://eprints.nottingham.ac.uk/31777/.

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Corn Hageman factor inhibitor (CHFI) is a bifunctional serine protease / α-amylase inhibitor protein having 127 residues and a molecular weight of 13.6-kDa. CHFI is selective toward FXIIa without affecting the function of the other coagulation factors. Coagulation FXII is a serine protease recognized to cause kinin generation and blood coagulation, cleaving plasma kallikrein and FXI. Results from FXII-deficient animal models proposed that this protein contributes to stable thrombosis that can cause obstruction of the blood vessels and its subsequent complications such as ischemic stroke. In contrast to other blood coagulation factors, deficiency in FXII is not related with haemorrhage in patients or in animals. These findings propose that specific inhibition of FXII could be an attractive medicine and a new method of anticoagulation to treat or prevent pathological thrombosis that could have a lower risk for bleeding and a safer anticoagulation profile than the currently available anticoagulants. Therefore, the current PhD project aimed at pharmacological investigation into CHFI-FXII interaction and FXII function at molecular level through the following objectives: first, developing an efficient expression and purification system for generating soluble and functional recombinant native type CHFI and establishing an inhibitory activity assay against FXIIa to verify the proper function of the recombinant protein. The second objective was testing the different recombinant variants of CHFI with the desired point mutations guided by a proper prediction study of CHFI-FXII interaction. The third was to investigate into the hypothesis of the tight-binding property of CHFI via different approaches of enzyme inhibition mechanisms and kinetic data analysis. The last objective was to investigate into the function of FXII by examining theeffect of Cys466 and glycosylated peptide remnant from the proline-rich region on the function of the catalytic domain via characterizing the different recombinant variants of the catalytic domain of FXIIa, FXIIc, FXIIac, HISTF-β FXII, and MBP-β-FXIIa. In the current study, an efficient system for soluble expression, single step purification and proper storage of functional, wild type rHIS-GST-CHFI was, for the first time, identified. The fully functional recombinant protein was verified via developing an inhibition test against FXIIa. The established expression, purification and inhibition assays were used as a fundamental guide to both generating and characterizing mutant proteins of interest that were made on the basis of an appropriate docking model of CHFI-FXIIa interaction. For the first time, the current investigation into the question of specificity of CHFI against FXII revealed that the central Arg34 at the very top of the fully exposed region of CHFI inhibition loop play a central role in the inhibition function of CHFI toward FXIIa. In addition, this study identified Trp22 at the N-terminus and Arg43 at the C-terminus of the central inhibition loop as two key interaction residues with FXIIa. It was also observed that, in the preinhibition test, CHFI behaves as a noncompetitive inhibitor. In contrast, it acts as a competitive inhibitor in the acute inhibition test, proposing that CHFI is a competitive inhibitor with slow degree of reversibility due to tightness of binding. Reversibility assay showed that CHFI is an inhibitor with slow degree of dissociation. The tight-binding property of CHFI could be due to a non-active site interaction and or numerous hydrogen bonds between the III key interaction residues and their potential targets on FXIIa. With respect to the investigation into FXII function, It was observed that both Cys340-Cys466 and glycosylated peptide fragment of the proline-rich region have a functional role for the full catalytic activity of FXII protease domain. Cumulatively, the current study identified the key important residues on the exposed surface of CHFI and their potential target residues on the surface of FXIIa that would be highly informative and important factors helping to understand the mechanism of selective and tight binding interaction of CHFI with FXIIa. This project can be considered as an early, necessary approach to design novel, specific and safe anticoagulants for the treatment of thrombosis and its complications.
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Chamberlain, Mitchell Sarah Ann Frances. "Chronic cough : an exploration of impact and an evaluation of non-pharmacological management in adults." Thesis, Keele University, 2016. http://eprints.keele.ac.uk/2371/.

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Chronic cough is defined as a cough that lasts for greater than 8 weeks in duration and has been estimated to have a prevalence of 11-13% of the population. Limited research has been conducted exploring its impact on the wider community. In up to 42% of chronic cough cases, the cough persists despite medical management, these cases tend to be labelled as refractory chronic cough. Pharmacological treatments are limited often with undesirable side effects. Research into non-pharmacological treatments for refractory chronic cough has been limited. An internet based European survey explored the impact of chronic cough (January 2012 - April 2013). A systematic review investigated the effectiveness of non-pharmacological interventions for refractory chronic cough. A single blinded multi-centre randomised controlled trial (RCT) investigated the efficacy of a non-pharmacological intervention (Physiotherapy, Speech and Language Therapy Interventions, - PSALTI) on cough related quality of life (QoL), cough frequency, severity, sensitivity, vocal performance, anxiety and depression alongside a control intervention. In total 1120 responses were collected and analysed from the European survey. Findings identified that cough impacted upon QoL, mood and ability to undertake activities and limited/ no effectiveness of medication; also a wish for more patient information to be available. PSALTI trial showed statistically significant differences between groups for the outcomes; QoL, cough frequency and urge to cough, improvements were significantly greater in the PSALTI group compared with control. There were no significant changes in outcomes from 4 weeks to 3 months suggesting that observed improvements were maintained. This thesis has identified the impact of chronic cough in Europe. It identified the need to improve the management of chronic cough and the information available for patients. This thesis also provides the first evidence within a single blinded multi-centre RCT that PSALTI is an effective treatment option for people with refractory chronic cough.
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Hassoni, Abdul-Nabi Atya. "Pharmacological studies on acetylcholine and other transmitter receptors from invertebrate muscle and central neurones." Thesis, University of Southampton, 1988. https://eprints.soton.ac.uk/335086/.

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Muscle tension recordings were made from earthworm body wall muscle and the action of acetylcholine, cholinomimtics and cholinolytics examined. The effect of cholinergic agents on muscle twitches induced following field stimulation was also investigated. Carbachol was 8 times more active than acetylcholine in the presence of physostigmine. α-Bungarotoxin, d-tubocurarine, gallamine, atropine, mecamylamine and hexamethonium reduced both electrical stimulation of the muscle and the acetylcholine response while β-bungarotoxin reduced the electrically induced twitch but enhanced the acetylcholine contraction. 0.4wM Hemicholinium abolished the electrically induced twitch while having no effect on the acetylcholine response, but at 4.0uiM, did reduce the acetylcholine response. These results provide further evidence for cholinergic excitatory innervation of earthworm body wall muscle. Intracellular recordings were made from identifiable central neurones of Helix aspersa and the action of anthelmintic compounds investigated. The anthelmintics pyrantel, morantel and deacylated amidantel mimicked acetylcholine induced excitation"D" and inhibition"H" had the same ionic mechanism and were blocked by d-tubocurarine. This suggests these compounds interact with acetylcholine receptors on Helix neurones. Levamisole only inhibited the activity. A series of glutamate analogues was tested on Helix neurones which were either excited or inhibited by Lglutamate. The only analogue with clear glutamate-1ike activity was thio-glutamic acid. In normal saline Lglutamate hyperpolarises the membrane potential of cell F-1. This event is chloride mediated and is reversed to a depolarisation followed by hyperpolarisation in low external chloride. This afterhyperpolarisation is reduced in sodium or potassium free saline or following application of strophanthidin, l.O-lOOyM. The local anaesthetics procaine and tetracaine mimicked the "H" and "D" effects of acetylcholine on certain neurones. Tetracaine, O.OlyM, gradually and reversibly reduced both "H" and "D" responses of acetylcholine and the "H" response to dopamine. This provides evidence that local anaesthetics can interact with responses linked to chloride, sodium and potassium ion channels.
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Seed, Alison. "Characterisation of the pharmacological actions in humans of multiple vasoactive enzyme inhibitors with therapeutic potential in heart failure." Thesis, Connect to e-thesis, 2007. http://theses.gla.ac.uk/119/.

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Thesis (M.D.) - University of Glasgow, 2007.
M.D. thesis submitted to the Faculty of Medicine, Dept. of Medicine and Therapeutics, University of Glasgow, 2007. Includes bibliographical references. Print version also available.
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Elbakay, Jamal Ali Mohamed. "Synthesis and pharmacological evaluation of novel anti-tumour prodrugs : synthesis and pharmacological investigations into novel MMP-activated peptide-based prodrugs of methotrexate as potential cancer therapeutics." Thesis, University of Bradford, 2017. http://hdl.handle.net/10454/15102.

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Methotrexate (MTX) is an antimetabolite anticancer agent that is used in treatment of multiple cancers, such as acute lymphoblastic leukaemia and osteosarcoma. A lack of selective tumour toxicity is one of the major problems associated with MTX chemotherapy, especially when given at high doses, as in high dose MTX (HDMTX) therapy. MTX causes various toxicity problems including life-threatening nephrotoxicity, haematological toxicity and neurotoxicity. Overcoming this toxicity is of great importance and has been attempted in various ways, not least via the design of prodrugs. The concept of tumour protease, and specifically matrix metalloproteinase (MMP), activated prodrugs was the focus of the work described in this thesis. This concept relies upon attachment of an MMP-sensitive peptide sequence to a specific site in a drug structure, so as to inactive it. The activity of the parent drug is restored once it is activated by the MMPs in the tumour microenvironment. In this work, different MMP-sensitive peptide sequences linked to MTX were synthesised, resulting in 63 MTX prodrugs. The MMP-mediated activation of these conjugates in tumour tissues (specifically HT1080 homogenates) ex vivo was assessed and the results were compared to the activation of these conjugates in various normal tissues specifically liver, kidney and lung. Specific criteria were established for the selection of promising conjugates for more detailed study. From 7 promising compounds, compound 75 was identified as the lead prodrug, demonstrating selective MMP activation, as indicated by inhibition of its activation by broad spectrum MMP inhibitor ilomastat. The pharmacokinetics of compound 75 was studied in tumour (HT1080) xenograft-bearing mice and the results were compared to those obtained from administration of equimolar doses of conventional MTX. Compound 75 led to enhanced tumour concentrations of MTX, with reduced exposure to normal tissues in vivo compared to conventional MTX therapy. Furthermore, the efficacy of equimolar doses of compound 75 and directly dosed MTX in reduction of HT1080 volume were compared. Superior antitumour activity was observed with compound 75 compared to MTX treatment. Compound 75 is the first example of an MMP-activated prodrug to be reported with enhanced therapeutic index, as evidenced by a full in vivo pharmacokinetic analysis and normal tissue metabolism data. The data presented in thesis support the concept of MMP-activated prodrug development, and form a strong foundation upon which to develop a clinicallyuseful MTX prodrug, with the potential to enhance efficacy and reduce toxicity to the patient.
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Elbakay, Jamal A. M. "Synthesis and pharmacological evaluation of novel anti-tumour prodrugs. Synthesis and pharmacological investigations into novel MMP-activated peptide-based prodrugs of methotrexate as potential cancer therapeutics." Thesis, University of Bradford, 2017. http://hdl.handle.net/10454/15102.

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Hafiz, Taghreed. "Molecular, biochemical and pharmacological characterisation of Mycobacterium tuberculosis cytochrome bd-I oxidase : a putative therapeutic target." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/12633/.

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Tuberculosis (TB) remains one of the most devastating diseases in humans. Nowadays, tuberculosis therapy is not sufficient to control the TB epidemic and only lasts for 6 months to cure patients and prevent relapse; therefore, the treatment of Mycobacterium tuberculosis (Mtb) is particularly challenging (1). New antibiotics, mainly those that are derived from new chemical classes, are more likely to be more effective against resistant strains. Moreover, expanding the knowledge of the mode of action of drugs has important implications in tackling TB. Only empirical approaches can be adopted in the journey of discovering new anti-tubercular drugs until a clear picture of latency and persister cells’ physiology is achieved. Mtb has the extraordinary ability to survive under hypoxia, suggesting a high degree of metabolic plasticity. The flexibility conferred by a modular respiratory system is critical to the survival of Mtb, thereby also making it a promising area of research for new drug targets. This thesis aimed towards the characterisation of cytochrome bd-I quinol oxidase (bd-I), a respiratory component that is believed to operate during both the replicative and “dormant” Mtb phenotypes. The essential nature of Mtb bd-I, which has no human homologue, has been confirmed in a recent deep sequencing study of genes required for Mtb growth by Griffin et al. (2), further confirming its potential as a novel target. Recombinant Mtb bd-I was successfully expressed under the control of the pUC19 lac promoter in the Escherichia coli ML16 bo3/bd-I and MB44 bo3/bd-I/bd-II knockout strains, allowing “noise-free” measurement of the enzyme. Initial steady-state kinetics of the enzyme was presented using a range of quinol substrates, revealing a substrate preference for dQH2 over Q1H2 and Q2H2. A number of bd-I inhibitors were identified and their pharmacodynamic profiles against Mtb H37Rv were determined. In addition, a pharmaco-metabolomics platform was initiated to explore the cellular response of Mtb to current first-line TB drugs as well as in house bd-I and type II NADH inhibitors. The initial findings are discussed in the context of the known mode of action of the drugs and future research needs in drug discovery of this devastating disease.
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Books on the topic "Therapeutics, pharmacological"

1

Goodman, Louis. The pharmacological basis of therapeutics. 8th ed. Maidenhead: McGraw-Hill, 1992.

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Cuello, A. Claudio. Pharmacological Mechanisms in Alzheimer's Therapeutics. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3.

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1906-, Goodman Louis Sanford, Brunton Laurence L, Chabner Bruce, and Knollmann Björn C, eds. Goodman & Gilman's pharmacological basis of therapeutics. New York: McGraw-Hill, 2011.

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Pharmacology and therapeutics for dentistry. 6th ed. St. Louis, Mo: Mosby Elsevier, 2011.

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1906-, Goodman Louis Sanford, Gilman Alfred 1908-, Brunton Laurence L, Lazo John S, and Parker Keith L, eds. Goodman & Gilman's the pharmacological basis of therapeutics. New York: McGraw-Hill, 2005.

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1906-, Goodman Louis Sanford, Hardman Joel G, Limbird Lee E, and Gilman Alfred Goodman 1941-, eds. Goodman & Gilman's the pharmacological basis of therapeutics. New York: McGraw-Hill, 2001.

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Pharmacogenomics in clinical therapeutics. Chichester, West Sussex, UK: Wiley-Blackwell, 2012.

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L, Brunton Laurence, and Goodman Louis Sanford 1906-, eds. The Goodman and Gilman's manual of pharmacological therapeutics. New York: McGraw-Hill, 2007.

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Goodman, Louis S. Goodman and Gilman's The pharmacological basis of therapeutics. 7th ed. New York: Macmillan, 1985.

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1906-, Goodman Louis Sanford, Gilman Alfred 1908-, and Gilman Alfred Goodman 1941-, eds. Goodman and Gilman's The pharmacological basis of therapeutics. 7th ed. New York: Macmillan, 1985.

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Book chapters on the topic "Therapeutics, pharmacological"

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Hall, N. D. "The pharmacological basis of antirheumatic drug therapy." In Therapeutics in Rheumatology, 3–48. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4899-2883-2_1.

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Cuello, A. Claudio. "Overview of the Alzheimer's Disease Pathology and Potential Therapeutic Targets." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 1–27. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_1.

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McGeer, Edith G., and Patrick L. McGeer. "Neuroinflammation, Alzheimer Disease, and Other Aging Disorders." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 149–66. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_10.

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Weggen, Sascha, Eva Czirr, Stefanie Leuchtenberger, and Jason Eriksen. "Nonsteroidal Anti-inflammatory Drugs (NSAIDs) and Derived Aβ42-Lowering Molecules for Treatment and Prevention of Alzheimer's Disease (AD)." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 167–93. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_11.

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Moreira, Paula I., Mark A. Smith, Xiongwei Zhu, Akihiko Nunomura, and George Perry. "The Potential Application of Antioxidant Agents in Alzheimer Disease Therapeutics." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 194–211. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_12.

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Poirier, Judes. "Apolipoprotein E: A Potent Gene-Based Therapeutic Target for the Treatment of Sporadic Alzheimer's Disease." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 212–22. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_13.

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Iqbal, Khalid, and Inge Grundke-Iqbal. "Tau Pathology as a Target in Alzheimer's Therapeutics." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 223–37. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_14.

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Estrada, Lisbell D., Cristian Lasagna, and Claudio Soto. "Design of Inhibitors of Amyloid-β Misfolding and Aggregation for Alzheimer's Therapy." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 238–54. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_15.

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Morissette, Céline, Diane Lacombe, Xianqi Kong, Ahmed Aman, Pascale Krzywkowski, Lioudmila Rodionova, Mounia Azzi, Daniel Delorme, and Barry D. Greenberg. "Potential Applications of Glycosaminoglycan-Related Compounds in Alzheimer's Disease." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 255–73. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_16.

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Schyf, Cornelis J. Van der, Werner J. Geldenhuys, and Moussa B. H. Youdim. "Multifunctional Neuroprotective Drugs for the Treatment of Alzheimer's Disease." In Pharmacological Mechanisms in Alzheimer's Therapeutics, 274–95. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-71522-3_17.

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Conference papers on the topic "Therapeutics, pharmacological"

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Albu, Diana I., Jiayi Wu, Kuan-chung Huang, Renee Wright-Michaud, Shanqin Xu, Galina Kuznetsov, Xingfeng Bao, and Mary Woodall-Jappe. "Abstract B198: Pharmacological profile of the PGE2EP4 receptor antagonist E7046." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b198.

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O'Connor, Mark J. "Abstract PL05-03: Exploiting cancer replication stress using pharmacological inhibitors of ATR and WEE1." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-pl05-03.

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Hou, Samuel, Stanislas Blein, Darko Skegro, Julie Macoin, Rami Lissilaa, and Jonathan Back. "Abstract C164: Preclinical pharmacological characterization of GBR 401, a new monoclonal antibody directed against human CD19." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c164.

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Ordentlich, Peter, Gloria Lee, Lori Kunkel, and Edward Sausville. "Abstract B196: Entinostat: A novel class 1 isoform selective histone deacetylase inhibitor (HDACi) with unique pharmacological properties." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b196.

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Viswanadha, Srikant, Meyyappan Muthuppalaniappan, Kanthikiran VS Varanasi, Sridhar Veeraraghavan, Josephrajan Thainashmuthu, Sivan Perumal Murugan, Prasad Babu Kakarla, Sumalatha Kuppireddi, and Swaroop Vakkalanka. "Abstract C212: Pharmacological and pharmacokinetc characterization of RP1040, a novel and potent c‐Met tyrosine kinase inhibitor." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-c212.

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Cassoux, Nathalie, Franck Assayag, Olfa Chouchane-Mlik, Jean-Jacques Fontaine, Fariba Nemati, Aurelie Thuleau, Olivia N'Doye, et al. "Abstract A20: Development and pharmacological assessment of new models of orthotopic primary human uveal melanoma and retinoblastoma xenografts." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a20.

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Basseville, Agnes, Akina Tamaki, Caterina Ierano, Yvona Ward, Robert W. Robey, Ramanujan Hegde, and Susan E. Bates. "Abstract 2610: Histone deacetylase inhibitors mediate pharmacological rescue of the ABCG2 Q141K variant: Potential for therapeutics in cancer and gout." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2610.

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Deplater, Ludmilla, Lamia Ouafi, Patricia de Cremoux, Olfa Chouchane-Mlik, Catherine Daniel, Leila Zemoura, Andre Nicolas, et al. "Abstract A15: Establishment and characterization of a new patient-derived non-small cell lung cancer xenograft panel for pharmacological assessment." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-a15.

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Trousil, Sebastian, Maciej Kalisczcak, Zachary Schug, Quang-De Nguyen, Giampaolo Tomasi, Rosy Favicchio, Diana Brickute, et al. "Abstract C118: Choline kinase inhibition with the novel pharmacological inhibitor ICL-CCIC-0019 reprograms cellular metabolism and inhibits cancer cell growth." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-c118.

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Chang, Ching-Wen, and Jeng-Fan Lo. "Abstract 4217: Targeting head and neck cancer-initiating cells with combinatorial therapeutics through pharmacological inhibition of ROS scavenger and conventional chemotherapy." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4217.

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Reports on the topic "Therapeutics, pharmacological"

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Basu, Sayani. Hyperbaric Oxygen Therapy: A Breakthrough in Healthcare. Science Repository Oü, December 2020. http://dx.doi.org/10.31487/sr.blog.22.

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The physiological and pharmacological benefits and high therapeutic response of hyperbaric oxygen therapy indicates that hyperbaric oxygen therapy offers promise in the treatment of a wide range of medical conditions.
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Determining the “IMPACT” of therapeutics for depression requires an adaptive trial design. ACAMH, August 2018. http://dx.doi.org/10.13056/acamh.10573.

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A large proportion of adolescents suffering from moderate-to-severe major depression respond to psychological and pharmacological therapy, and the range of effective treatment modalities is increasing. Now, Ian Goodyer and Paul Wilkinson have compiled a Practitioner Review that compares the various treatment options available and assesses their effectiveness for adolescents affected by major depressive episodes.
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