Готові списки джерел за темами / Treatment targets

Добірка наукової літератури з теми "Treatment targets"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Treatment targets"

1

Davies, Nick, Tim Peakman, and Steve Arlington. "From targets to targeted treatment solutions." Drug Discovery Today 9, no. 6 (March 2004): 245–47. http://dx.doi.org/10.1016/s1359-6446(03)02915-5.

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2

Simon, Richard. "Targets for treatment success." Nature Clinical Practice Oncology 3, no. 1 (January 2006): 1. http://dx.doi.org/10.1038/ncponc0402.

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3

Bradbury, Jane. "Potential atherosclerosis treatment targets?" Lancet 353, no. 9161 (April 1999): 1334. http://dx.doi.org/10.1016/s0140-6736(05)74331-2.

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4

Lipworth, B. J. "Targets for inhaled treatment." Respiratory Medicine 94 (September 2000): S13—S16. http://dx.doi.org/10.1016/s0954-6111(00)80135-3.

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5

LIPWORTH, B. "Targets for inhaled treatment." Respiratory Medicine 94 (September 2000): S13—S16. http://dx.doi.org/10.1016/s0954-6111(00)90118-5.

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6

Goadsby, PeterJames, David Moreno-Ajona, and MaríaDolores Villar-Martínez. "Emerging Targets for Migraine Treatment." Neurology India 69, no. 7 (2021): 98. http://dx.doi.org/10.4103/0028-3886.315989.

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7

Field, Benjamin C. T., Owais B. Chaudhri, and Stephen R. Bloom. "Obesity treatment: novel peripheral targets." British Journal of Clinical Pharmacology 68, no. 6 (December 2009): 830–43. http://dx.doi.org/10.1111/j.1365-2125.2009.03522.x.

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8

Otto, Grant. "Novel targets for itch treatment." Nature Reviews Drug Discovery 18, no. 9 (July 19, 2019): 666. http://dx.doi.org/10.1038/d41573-019-00126-4.

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9

Khanna, Reena, and Vipul Jairath. "Treatment Targets in Ulcerative Colitis." Gastroenterology 151, no. 5 (November 2016): 1030–32. http://dx.doi.org/10.1053/j.gastro.2016.09.028.

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10

Lillegraven, Siri, and Espen A. Haavardsholm. "Subclinical Treatment Targets in Rheumatology." Rheumatic Disease Clinics of North America 45, no. 4 (November 2019): 593–604. http://dx.doi.org/10.1016/j.rdc.2019.07.007.

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Дисертації з теми "Treatment targets"

1

Ajmo, Craig T. "Alternative targets for the treatment of stroke." [Tampa, Fla.] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0002114.

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2

Ajmo, Craig T. Jr. "Alternative Targets for the Treatment of Stroke." Scholar Commons, 2007. https://scholarcommons.usf.edu/etd/594.

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Анотація:
Stroke is cerebrovascular injury that has been reported to be the third leading cause of death and the first leading cause of disability in the world (W. H.O. 2007). Currently, there is only one FDA approved treatment for stroke which is recombinant tissue plasminogen activator. This treatment has a narrow therapeutic window of three hours after ischemic stroke and can adversely cause the production of oxygen free radicals and intracranial hemorrhage. These limitations result in only 2-3% of all stroke victims as being candidates for this therapy as many patients do not arrive at the hospital in time to receive treatment, are not properly diagnosed, or do not know that they have had a stroke within this three hour time period. The purpose of these experiments was to elucidate alternative targets of stroke for the benefit of developing new treatments that stimulate neuroprotective and anti-inflammatory effects at the site of injury. It has been shown that transfusion of human umbilical cord blood cells up to 48 hours after stroke significantly reduces infarction and we have examined other targets that mimic these effects. We have shown that sigma receptor activation by DTG, a high affinity universal sigma agonist, reduces infarct volume when administered 24 hours after stroke. This suggests that modulation of neurodegenerative and inflammatory responses can extend the therapeutic window of treatment. For the first time, evidence is provided that shows that the spleen enhances the neurodegeneration caused by stroke as splenectomy prior to stroke profoundly decreased infarction volume. Finally, we studied signaling mechanisms of the splenic reaction to stroke and determined that this response is not directly dependent on neurotransmission via the splenic nerve. Denervation of the spleen prior to stroke showed no changes in neurodegenerative load at the site of injury in rat brains when compared to those subjected to stroke only. Overall, these experiments provide evidence showing that targets mediating neuroprotective and anti-inflammatory effects can lead to novel therapeutic interventions of stroke.
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3

Yue, Lok-man, and 庾樂民. "Therapeutic targets of arsenic trioxide in lymphoma treatment." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/197540.

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Lymphomas are malignant diseases involving the lymphatic system. Arsenic trioxide (As2O3) is a current therapeutic agent for acute promyelocytic leukaemia (APL).APL cells are sensitive to As2O3, with As2O3directly targeting the PML-RARA protein that plays an important role in the oncogenesis of APL. In order to discover the potential of As2O3as a treatment of lymphoma, understanding of the molecular mechanism of As2O3in human lymphoma cells is essential. In this thesis, we showed that the MYC gene is a therapeutic target for As2O3in B-cell lymphomas and the CCND1 (cyclin D1) gene is another therapeutic target for As2O3in mantle cell lymphoma (MCL), a subtype of non-Hodgkin lymphoma (NHL). Both real-time RT-PCR and immunoblotting analysis showed that the expression levels of MYC in all B-cell lymphoma cell lines were down-regulated at both mRNA and protein level after As2O3treatment. The expression levels of MYC were also found to positively correlate with the arsenic sensitivity as measured by MTT assay. Hence, the higher the level of MYC expression, the higher the arsenic sensitivity of human B-cell lymphoma cell lines. Besides, the change of downstream genes after modulation of MYC expression level by As2O3 treatment was investigated. The expression level of CDKN1A and CDKN1B was increased after As2O3 treatment. Interestingly, the growth rate of MYC over-expressing lymphoma cell lines decreased significantly after As2O3treatment, while there was no significant decrease in colony formation assay in lymphoma cells without MYC over-expression. Immunoblotting analysis showed that As2O3could degrade the cyclin D1 protein in mantle cell lymphoma cell lines in a dose-dependent manner. Real-time RT-PCR analysis also showed that the mRNA level of CCND1gene was decreased after As2O3treatment. We also demonstrated that As2O3-induced cyclin D1 protein degradation was related to the proteasome pathway. The growth rate of MCL cell line decreased significantly after As2O3treatmentby using colony formation assay. Human water channel protein, aquaporin 9 (AQP9) has been demonstrated to facilitate the arsenic uptake in human leukaemia cells. In this thesis, we showed that the expression levels of AQP9were found to positively correlate with the arsenic sensitivity as measured by MTT assay in B-cell lymphoma cells. We also demonstrated that dexamethasone could up-regulate AQP9expressions at both mRNA and protein levels in human B-cell lymphoma cell lines. These results not only suggest that As2O3is a potential therapy for B-cell lymphomas, especially for those MYC-over-expressed B-cell lymphomas and MCL, but also indicate that MYC may act as a biomarker for predicting the clinical behaviour of B-cell lymphoma patients to the As2O3treatment.Moreover, dexamethasone pre-treatment may enhance the therapeutic effect of As2O3by up-regulating AQP9expression in B-cell lymphomas.
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Medicine
Master
Master of Philosophy
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4

Aziz, Abdul Maruf Asif. "Neuropeptide Receptors as Treatment Targets in Alcohol Use Disorders." Doctoral thesis, Linköpings universitet, Centrum för social och affektiv neurovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-139884.

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Анотація:
Alcohol use disorder (AUD) is a complex disorder with multiple pathophysiological processes contributing to the initiation, progression and development of the disease state. AUD is a chronic relapsing disease with escalation of alcohol-intake over time in repeated cycles of tolerance, abstinence and relapse and hence, it is very difficult to treat. There are only a few currently available treatments with narrow efficacy and variable patient response. Thus it is important to find new, more effective medications to increase the number of patients who can benefit from pharmacological treatment of AUD. The research presented in this thesis work focuses on the critical involvement of central neuropeptides in alcohol-related behaviors. The overall aim was to evaluate the nociceptin/orphanin FQ (NOP) receptor, the neuropeptide Y (NPY) Y2 receptor and the melanin-concentrating hormone (MCH) receptor 1 as novel and potential pharmacological treatment targets for AUD by testing the NOP receptor agonist SR-8993, the NPY-Y2 receptor antagonist CYM-9840 and the MCH1 receptor antagonist GW803430 in established animal models. In the first study (Paper I), the novel and selective NOP agonist SR-8993 was assessed in rat models of motivation to obtain alcohol and relapse to alcohol seeking behavior using the operant self-administration (SA) paradigm. Firstly, treatment with SR-8993 (1 mg/kg) showed a mildly anxiolytic effect and reversed acute alcohol withdrawal-induced “hangover” anxiety in the elevated plus-maze (EPM). Next, it potently attenuated alcohol SA and motivation to obtain alcohol in the progressive ratio responding (PRR) and reduced both alcohol cue-induced and yohimbine stress-induced reinstatement of alcohol seeking, without affecting the pharmacology and metabolism of alcohol nor other control behaviors. To extend these findings, SR-8993 was evaluated in escalated alcohol-intake in rats.  Treatment with SR-8993 significantly suppressed alcohol-intake and preference in rats that were trained to consume high amounts of alcohol in the two-bottle free choice intermittent access (IA) paradigm. SR-8993 also blocked operant SA of alcohol in rats that showed robust escalation in operant alcohol SA following chronic IA exposure to alcohol. In the second study (Paper II), SR-8993 was further evaluated in a model for escalated alcohol-intake induced by long-term IA exposure to alcohol. The effect of previous experience on operant alcohol SA on two-bottle free choice preference drinking was evaluated and sensitivity to treatment with SR-8993 was tested in rats selected for escalated and non-escalated alcohol seeking behavior. We found that rats exposed to the combined SA-IA paradigm showed greater sensitivity to SR-8993 treatment. In addition, acute escalation of alcohol SA after a three-week period of abstinence was completely abolished by pretreatment with SR-8993. In the third study (Paper III), the effects of the novel, small molecule NPY-Y2 antagonist CYM-9840 were tested in operant alcohol SA, PRR which is a model for motivation to work for alcohol and reinstatement of alcohol-seeking behavior. Treatment with CYM-9840 (10 mg/kg) potently attenuated alcohol SA, progressive ratio responding and stress-induced reinstatement using yohimbine as the stressor, while alcohol cue-induced reinstatement was unaffected. Moreover, a range of control behaviors including taste sensitivity, locomotor and pharmacological sensitivity to the sedative effects of alcohol remained unaffected by CYM-9840 pretreatment, indicating that its effects are specific to the rewarding and motivational aspects of alcohol-intake and related behaviors. CYM-9840 also reversed acute alcohol withdrawal-induced “hangover” anxiety measured in the EPM and reduced alcohol-intake in the 4 hour limited access two-bottle free choice preference drinking model. Finally, in the fourth study (Paper IV), the selective MCH1-R antagonist GW803430 was tested in rat models of escalated alcohol-intake. Pretreatment with GW803430 (effective at 10 & 30 mg/kg) dose-dependently reduced alcohol and food-intake in rats that consumed high amounts of alcohol during IA, while it only decreased food-intake in rats that consumed low amounts of alcohol during IA, likely due to a floor effect. Upon protracted abstinence following IA, GW803430 significantly reduced operant alcohol SA and this was associated with adaptations in MCH and MCH1-R gene-expression. In contrast, GW803430 did not affect escalated alcohol SA induced by chronic alcohol vapor exposure and this was accompanied by no change in MCH or MCH1-R gene expression. Overall, these results suggest that the MCH1-R antagonist affects alcohol-intake through regulation of both motivation for caloric-intake and the rewarding properties of alcohol. In conclusion, our results suggest critical roles for these central neuropeptides in the regulation of anxiety and of alcohol reward, making them potential pharmacological targets in the treatment of AUD.
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5

Cozzi, Sarah-Jane. "Molecular targets of anticancer PKC activators in the treatment of melanoma /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19185.pdf.

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6

Moilanen, A. M. (Anne-Mari). "Identification of novel drug targets for the treatment of heart failure." Doctoral thesis, Oulun yliopisto, 2012. http://urn.fi/urn:isbn:9789514299131.

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Abstract Heart failure (HF) is a complex pathological state, involving simultaneous alterations in several signalling pathways and changes in gene programming. In HF, activation of the neurohumoral factors and renin-angiotensin-aldosterone (RAA) system occurs as a compensatory mechanism to combat the abnormal ventricular function. Developments in cardiac gene delivery methods have exerted a significant impact to treat HF and to discover the novel molecular mechanisms associated with HF and other cardiac diseases. This study demonstrated that adenovirus–mediated gene delivery of B-type natriuretic peptide (BNP) into the anterior wall of the left ventricle decreased myocardial fibrosis and increased capillary density. Post-infarction BNP improved systolic function associated with normalization of cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA) 2 expression and phospholamban phosphorylation at Thr17. On the other hand, (Pro)renin receptor ([P]RR) gene delivery resulted deleterious effects on cardiac function and (P)RR activation induced distinct angiotensin II (Ang II)-independent extracellular matrix remodelling and worsening of cardiac function. (P)RR gene delivery resulted in Ang II-independent activation of extracellular-signal regulated (ERK1/2) phosphorylation and increased myocardial fibrosis. In conclusion, the present study indicates that myocardial BNP gene delivery can achieve pleiotropic, context-dependent, favourable effects on cardiac function and that BNP can act locally as a mechanical load–activated regulator of angiogenesis and fibrosis. These results also implicate that (P)RR blockers may display additional cardiac effects in addition to its ability to evoke effective RAA system blockade. Overall, the findings of this study provide a better understanding of the molecular mechanisms involved in the biological actions of BNP and (P)RR, and identify BNP and (P)RR as potential novel drug targets for the treatment of HF
Tiivistelmä Neuroendokriinisellä aktivaatiolla, jonka seurauksena aiheutuu muun muassa verisuonten supistumista ja laajenemista sekä nesteen kertymistä elimistöön, on tärkeä merkitys sydämen vajaatoiminnan kehittymisessä. Neuroendokriininen aktivaatio kompensoi sydämen vajaatoiminnan seurauksena tapahtuvaa kammioiden poikkeavaa toimintaa. Yksi keskeisimmistä verisuonia supistavista tekijöistä on reniini-angiotensiini-aldosteroni (RAA) -järjestelmä, ja verisuonia laajentaviin tekijöihin kuuluvat muun muassa natriureettiset peptidit, kuten B-tyypin natriureettinen peptidi (BNP) ja A-tyypin natriureettinen peptidi. Geeninsiirtomenetelmillä on ollut merkittäviä vaikutuksia uusien hoitomenetelmien kehittämisessä, sydämen vajaatoiminnan syiden selvittämisessä ja uusien kohdegeenien tunnistamisessa sydämen vajaatoiminnan hoitoon. Väitöskirjan tutkimustulokset osoittivat, että suora adenovirusvälitteinen geeninsiirto rotan sydämen vasemman kammion etuseinään on toimiva menetelmä uusien kohdegeenien löytämiseksi sydämen vajaatoiminnan hoitoon. BNP:n geeninsiirto vähensi merkitsevästi fibroosin muodostumista ja lisäsi verisuonten uudismuodostumista sydämessä. Sydäninfarktin jälkeen BNP paransi sydämen systolista toimintaa, johon liittyi aktiivisen kalsiumpumpun, SERCA2:n ja fosfolambaani-proteiinin fosforylaation normalisoituminen. (Pro)reniini reseptorin ([P]RR) geeninsiirto aiheutti angiotensiini II:sta riippumatonta solunulkoisen matriksin uudelleenmuotoutumista ja sydämen toiminnan huonontumista sekä lisääntynyttä sydämen fibroosia. Väitöskirjatutkimus antaa uutta tietoa solunsisäisistä molekulaarisista mekanismeista sydänsoluissa. BNP geeninsiirto aiheutti sydämen tautitilasta riippuvia suotuisia tapahtumia, ja se toimi paikallisesti muun muassa fibroosia ehkäisevänä tekijänä. (P)RR geeninsiirtotulosten perusteella voidaan olettaa, että (P)RR:n salpaus saattaa olla uusi tehokas hoitokeino sydämen vajaatoiminnan hoitoon
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7

Lam, Chi-leung David, and 林志良. "Oncogenic mutations as biomarkers and therapeutic targets in lung cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207610.

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Oncogenic mutations in lung cancer further our knowledge about cancer initiation and progression, and may guide personalized treatment. The fact that targeted therapy is most effective in subsets of patients with defined molecular targets indicates the need for classification of clinically-related molecular tumor phenotypes based on the presence of oncogenic mutations, including EGFR mutations and EML4-ALK rearrangements. The identification of EGFR mutations, in up to half of lung adenocarcinomas in Asians, could predict clinical sensitivity to tyrosine kinase inhibitor (TKI). However, testing for mutations is not always possible due to tumor tissue availability. The therapeutic decision sometimes remains a clinical one especially for elderly lung cancer patients but no known mutation status. We studied the survival outcomes of targeted therapy versus conventional chemotherapy in elderly patients with lung cancer when we did not yet have routine EGFR mutation testing and demonstrated comparable survival outcomes in targeted therapy compared to chemotherapy, implying that survival with targeted therapy could be better if the treatment population could be selected with EGFR mutations. Though testing for EGFR mutation in tumor biopsy have later become routine practice and remains the accepted reference for therapeutic decision, the detection of EGFR mutations in plasma DNA with high diagnostic performance will be useful adjunct for diagnostic and therapeutic monitoring. Among patients with EGFR mutations in tumor biopsy, the concurrent detection of EGFR mutation in plasma DNA was found to confer a less favorable prognosis in terms of overall survival than those patients with EGFR mutations in tumor biopsy but the corresponding mutation was not detected in plasma. Other oncogenic mutations with therapeutic implications in lung tumors are yet to be fully explored, like ALK, KRAS, ROS1 or NTRK1 mutations. It is not exactly the tumor – but the mutations in the tumor that need to be explored with reference to clinical behavior. Even with EGFR mutation with well-established clinical implications, further exploration into its mechanistic functions will help in understanding of drug resistance. Lung cancer cell lines established from patients with known mutation profiles could be useful tools for studying the biology of known molecular targets as well as for therapeutic testing. Four new lung adenocarcinoma and one mesothelioma cell lines were established from patients with different clinical characteristics and oncogenic mutation profiles. These cell lines with defined mutation profiles will provide tools for exploration of lung cancer and mesothelioma biology with respect to molecular therapeutic targets. The Large Tumor Suppressor 2 (LATS2) gene was a differentially expressed gene between EGFR mutant and wildtype lung adenocarcinomas. The differential LATS2 expression levels were predictive of survival in patients with resected lung AD and may modulate tumor growth via different signaling pathways in EGFR mutant and wild-type tumors. The identification of oncogenic mutations has led to a new paradigm of targeted therapy in lung cancer. Further improvements in outcome of lung cancer management will stem from research into the biology of oncogenic mutations and their clinico-pathological correlations, which would fuel parallel development of clinically efficacious targeted therapies.
published_or_final_version
Medicine
Master
Doctor of Medicine
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8

Weist, Mark D. "Empirical validation of treatment targets for the management of diabetes in children." Diss., Virginia Tech, 1991. http://hdl.handle.net/10919/39865.

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9

Murabito, Ettore. "Application of differential metabolic control analysis to identify new targets in cancer treatment." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/application-of-differential-metabolic-control-analysis-to-identify-new-targets-in-cancer-treatment(3a9b75ba-027d-449b-af38-263341953418).html.

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In the quest for anti-cancer drugs with high efficacy and low toxicity, cancer metabolism has increasingly been a focus of interest in clinical research. Enhanced glycolysis and robust production of lactate constitute characteristic traits that discriminate many cancerous cells from their normal counterparts. This, in principle, may provide researchers with a general handle on such a complex disease, regardless of the intrinsic genotypic heterogeneity of the single transformed cells. The work carried out during this project and presented in this thesis consists of developing and applying analytical approaches, mainly drawn from the field of metabolic control analysis (MCA), to the study of cancer metabolism. The ultimate goal is to assess whether, and to what extent, the metabolic features of cancer cells may be exploited in the attempt to attack the malignancy more specifically than through traditional clinical approaches. The underlying idea consists of identifying enzymes that represent points of fragility specifically characterising the cancerous metabolic phenotype. These enzymes are such that an alteration in their activity (due for example to the action of an anticancer drug) would elicit the desired response in cancer cells, without affecting their normal counterparts. The application of MCA relies on a mathematical representation of the system under study. Creating such a model is often hampered by the lack of data about the precise kinetic laws governing the different reaction steps and the value of their corresponding parameters. The most important result reached during this project shows that the metabolic quantities defining the normal and cancer phenotypes (such as fluxes and metabolite concentrations), together with heuristic assumptions about the properties of typical enzyme-catalyzed reactions, already allow for a fast and efficient way to explore the effectiveness of putative drug targets with respect to criteria of high efficacy and low toxicity. The relevance of this result lies in the fact that the quantities defining a metabolic phenotype are experimentally more accessible than the kinetic parameters of the different enzymatic steps in the system.
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10

D'Costa, Z. C. "The identification of novel therapeutic targets for the treatment of TBX2-driven breast cancers." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546040.

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Книги з теми "Treatment targets"

1

Canales, Juan. Emerging targets for drug addiction treatment. Hauppauge, N.Y: Nova Science Publisher's, 2012.

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2

Stock, Christian, and Luis A. Pardo, eds. Targets of Cancer Diagnosis and Treatment. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-03994-2.

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3

Paul-Peter, Tak, ed. New therapeutic targets in rheumatoid arthritis. Basel: Birkhäuser, 2009.

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4

Treatment protocols in communicative disorders: Targets and strategies. Austin, Tex: Pro-ED, 1998.

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5

Foundation, Novartis, ed. Heart failure: Molecules, mechanisms and therapeutic targets. Chichester: John Wiley, 2006.

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6

Holgate, S. T., and Riccardo Polosa. Asthma: Modern therapeutic targets. Oxford: Clinical Pub., 2007.

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7

HIV/AIDS, Joint United Nations Programme on. What countries need: Investments needed for 2010 targets. Geneva: UNAIDS, 2009.

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8

Godfrey, Christine. A health strategy for alcohol: Setting targets and choosing policies. York: Centre for Health Economics, University of York, 1992.

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9

Godfrey, Christine. A health strategy for alcohol: Setting targets and choosing policies. York: York University, Centre for Health Economics, 1992.

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10

Gaestel, Matthias, and K. Asadullah. Kinase targets and inhibitors in inflammation, 2007. Trivandrum, India: Transworld Research Network, 2007.

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Частини книг з теми "Treatment targets"

1

Tu, Shi-Ming. "Cancer Targets." In Cancer Treatment and Research, 115–28. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-5968-3_11.

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2

Poulter, Neil R. "Current treatment targets." In Clinical Manual of Total Cardiovascular Risk, 57–64. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84800-253-1_4.

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3

Farley, John, and Michael J. Birrer. "Novel Therapeutic Targets." In Cancer Treatment and Research, 63–84. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-98094-2_3.

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4

Clouser, Mary, Lisa M. Hess, and Setsuko K. Chambers. "Biomarker Targets and Novel Therapeutics." In Cancer Treatment and Research, 85–105. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-98094-2_4.

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5

Deutsch, Stephen I., Barbara L. Schwartz, Richard B. Rosse, John Mastropaolo, Ayman H. Fanous, Abraham Weizman, Jessica A. Burket, and Brooke L. Gaskins. "Schizophrenia Endophenotypes as Treatment Targets." In The Handbook of Neuropsychiatric Biomarkers, Endophenotypes and Genes, 113–22. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9464-4_7.

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6

Vamvini, Maria, and Florence M. Brown. "Targets and Rationale for Treatment." In Comprehensive Clinical Approach to Diabetes During Pregnancy, 149–88. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-89243-2_9.

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Page, C. P., and D. Spina. "Phosphodiesterase Inhibitors in the Treatment of Inflammatory Diseases." In Phosphodiesterases as Drug Targets, 391–414. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17969-3_17.

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Deer, Timothy R., and Jason E. Pope. "Innovative Central Neuromodulation Targets for Pain." In Treatment of Chronic Pain Conditions, 221–22. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6976-0_63.

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Rahmé, Ramy, Cécile Esnault, and Hugues de Thé. "Molecular Targets of Treatment in APL." In Acute Promyelocytic Leukemia, 17–27. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-64257-4_2.

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Palomares, Sara Morales, and Marilyn J. Cipolla. "Vascular Targets for Ischemic Stroke Treatment." In Translational Stroke Research, 3–36. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9530-8_1.

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Тези доповідей конференцій з теми "Treatment targets"

1

Solov'eva, E. A., and D. S. Tarasov. "Membrane technology in biological wastewater treatment." In SCIENCE OF RUSSIA: TARGETS AND GOALS. "Science of Russia", 2019. http://dx.doi.org/10.18411/sr-10-12-2019-08.

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2

Ajmagambetov, M. ZH, N. B. Omarov, E. O. Masalimov, D. B. Auzhanov, S. K. Bajzakova, and K. T. Karibaev. "Our experience in the treatment of diffuse toxic and nodular goiter." In SCIENCE OF RUSSIA: TARGETS AND GOALS. ЦНК МОАН, 2020. http://dx.doi.org/10.18411/sr-10-04-2020-18.

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3

Inês, Luís. "24 Disease activity and treatment targets in SLE." In 11th Annual Meeting of the Lupus Academy, Hybrid meeting held 8–10th April 2022 in Florence, Italy. Lupus Foundation of America, 2022. http://dx.doi.org/10.1136/lupus-2022-la.24.

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4

dos Anjos, Carolina, Fabio C. Pogliani, Fábio P. Sellera, Maurício Baptista, Martha S. Ribeiro, Nilton Lincopan, Milena Dropa, and Caetano Sabino. "Distinct targets for blue light photoinactivation (Conference Presentation)." In Photonic Diagnosis, Monitoring, Prevention, and Treatment of Infections and Inflammatory Diseases 2020, edited by Tianhong Dai, Mei X. Wu, and Jürgen Popp. SPIE, 2020. http://dx.doi.org/10.1117/12.2547336.

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Solov'eva, E. A., and V. S. Kim. "Modern approaches to the selection and calculation of aeration systems for biological wastewater treatment." In SCIENCE OF RUSSIA: TARGETS AND GOALS. "Science of Russia", 2019. http://dx.doi.org/10.18411/sr-10-12-2019-07.

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Keustermans, Johannes, Stijn De Buck, Hein Heidbüchel, and Paul Suetens. "Automated planning of ablation targets in atrial fibrillation treatment." In SPIE Medical Imaging, edited by Benoit M. Dawant and David R. Haynor. SPIE, 2011. http://dx.doi.org/10.1117/12.878250.

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Kim, Hyoung, Erin George, Haineng Xu, Sergey Medvedev, Veena Jagannathan, Mark Morgan, Gordon Mills, Eric Brown, and Fiona Simpkins. "Abstract AP31: ATR INHIBITION TARGETS TREATMENT RESISTANT OVARIAN CANCER." In Abstracts: 12th Biennial Ovarian Cancer Research Symposium; September 13-15, 2018; Seattle, Washington. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1557-3265.ovcasymp18-ap31.

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Ajmagambetov, M. ZH, N. B. Omarov, S. T. Abdrahmanov, A. ZH Ahmetov, A. B. Rahmetullin, and E. Ә. Mұқash. "The results of surgical treatment of patients with gallstone disease over last 5 years according to the clinic." In SCIENCE OF RUSSIA: TARGETS AND GOALS. ЦНК МОАН, 2020. http://dx.doi.org/10.18411/sr-10-04-2020-17.

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Song, X., L. Ye, and M. Jin. "Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment: A System Review." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4970.

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Noriega, Ricardo, Jeyshka Reyes, Blanca Quiñones, Joseline Serrano, Pablo Vivas, and Josué Pérez. "Abstract A57: Identification of novel targets for ovarian cancer treatment." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a57.

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Звіти організацій з теми "Treatment targets"

1

Zhang, Xiao-kun. Immediate-Early Response Genes as Targets for Breast Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405234.

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2

Liberzon, Israel, and Sophie A. George. Identifying Molecular Targets For PTSD Treatment Using Single Prolonged Stress. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612301.

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3

Liberzon, Israel, and Sophie A. George. Identifying Molecular Targets for PTSD Treatment Using Single Prolonged Stress. Fort Belvoir, VA: Defense Technical Information Center, October 2015. http://dx.doi.org/10.21236/ada624616.

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4

Mar, Brenton G. Novel Membrane-Associated Targets for Diagnosis and Treatment of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada427373.

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Mar, Brenton G., and Carol A. Westbrook. Novel Membrane-Associated Targets for Diagnosis and Treatment of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417511.

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6

Perrimon, Norbert. Parallel Genomic and Chemical Screens to Identify Both Therapeutic Targets and Inhibitors of These Targets in the Treatment of Neurofibromatosis. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada465264.

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Westbrook, Carol A. Novel Targets for Diagnosis and Treatment of Breast Cancer Identified by Genomic Analysis. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada419634.

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Westbrook, Carol A. Novel Targets for the Diagnosis and Treatment of Breast Cancer Identified by Genomic Analysis. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada463839.

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9

Bakel, Allen J., Cliff Conner, Kevin Quigley, and George F. Vandegrift. Waste Treatment of Acidic Solutions from the Dissolution of Irradiated LEU Targets for 99-Mo Production. Office of Scientific and Technical Information (OSTI), October 2016. http://dx.doi.org/10.2172/1328741.

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10

Sabatini, David. Identifying Novel Drug Targets for the Treatment of Tuberous Sclerosis Complex Using High Throughput Technologies. Addendum. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada473385.

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