subject:(pharmacology)

UCLA

1. Cohen, Alexa Nichelle. Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate.

Degree: Molecular and Medical Pharmacology, 2015, UCLA

URL: http://www.escholarship.org/uc/item/37p2f58x

► Prostatic adenocarcinomas can recur with aggressive and lethal small cell neuroendocrine carcinoma (SCNC). Since glycolysis is a feature of malignancy and the degree generally correlates… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Cohen, A. N. (2015). Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/37p2f58x

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cohen, Alexa Nichelle. “Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate.” 2015. Thesis, UCLA. Accessed March 07, 2021. http://www.escholarship.org/uc/item/37p2f58x.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cohen, Alexa Nichelle. “Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate.” 2015. Web. 07 Mar 2021.

Vancouver:

Cohen AN. Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate. [Internet] [Thesis]. UCLA; 2015. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/37p2f58x.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cohen AN. Glucose Metabolism and CD44 in Small Cell Neuroendocrine Carcinoma of the Prostate. [Thesis]. UCLA; 2015. Available from: http://www.escholarship.org/uc/item/37p2f58x

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

UCLA

2. Zhang, Jin. The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function.

Degree: Pharmacology, 2016, UCLA

URL: http://www.escholarship.org/uc/item/5qr271m5

► BKCa channels are widely expressed ion channels and characterized by their large conductance to potassium and sensitivity to calcium and voltage. It is typically observed… (more)

▼ BKCa channels are widely expressed ion channels and characterized by their large conductance to potassium and sensitivity to calcium and voltage. It is typically observed at the plasma membrane in the majority of cell types, with adult cardiomyocytes being an exception. Previously, both electrophysiological and immunological studies have detected BKCa channels in cardiomyocytes mitoplasts, confirming the presence of this K+ channel (mitoBKCa); however, its physiological functions have not yet fully understood. This work is the first one to examine the interactome of mitoBKCa channels in adult heart (isolated cardiomyocytes and whole ventricle). We used a directed proteomic approach aided by co-immunoprecipitation with BKCa antibodies and pull-down with recombinant DEC sequences. As a result, we identified an extensive network of the mitoBKCa, channel and overall, a total of 1079 different proteins were identified as partners of the BKCa channel in cardiomyocytes and left ventricle, including 151 mitochondrial proteins. Two putative protein partners were selected to validate and further examine the associations with BKCa channels: i) the Tom22 from the mitochondrial import system, and ii) the adenine nucleotide translocator (ANT), which is linked to oxidative phosphorylation and the regulation of mPTP.We first demonstrated the interactions of mitoBKCa with Tom22 through reciprocal co-immunoprecipitation (CO-IP), and then further confirmed that both Tom22 and BKCa were targeted into mitochondria through cell fractionation. This result raises the possibility of the functional interaction between the two proteins in mitochondria, supporting a potential import mechanism of BKCa channel through Tom22. Additionally, we identified the transmembrane domain of BKCa channel (1-711) as the main interacting regions with Tom22 through CO-IP. Next, we verified and studied the interactions between mitoBKCa and ANT with similar approaches. As a result, mitoBKCa was able to co-immunoprecipitate ANT, and the presence of DEC sequence in BKCa-DEC enhanced the ability of ANT to associate with BKCa by ~30%. More importantly, this interaction has a very high likelihood to happen in the mitochondria, as supported by the cell fractionation experiment that the majority of ANT and a considerate amount of mitoBKCa were targeted into mitochondria. This finding indicates a molecular link between mitoBKCa and mPTP, as ANT acts like an important regulatory component of it. Furthermore, the transmembrane domain of BKCa (1-343) can also contribute to the molecular interaction between BKCa channel and ANT.

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Zhang, J. (2016). The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/5qr271m5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zhang, Jin. “The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function.” 2016. Thesis, UCLA. Accessed March 07, 2021. http://www.escholarship.org/uc/item/5qr271m5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zhang, Jin. “The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function.” 2016. Web. 07 Mar 2021.

Vancouver:

Zhang J. The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function. [Internet] [Thesis]. UCLA; 2016. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/5qr271m5.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zhang J. The subproteome of mitoBKCa channels from cardiomyocytes reveals novel insights into its mitochondrial import mechanism and function. [Thesis]. UCLA; 2016. Available from: http://www.escholarship.org/uc/item/5qr271m5

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – San Diego

3. Yu, Olivia. GPCR and RhoA-Mediated Transcriptional Regulation.

Degree: Biomedical Sciences, 2016, University of California – San Diego

URL: http://www.escholarship.org/uc/item/98d4j5cs

► The ability of a subset of G-protein coupled receptors (GPCRs) to activate RhoAendows them with unique growth regulatory properties. Dysregulation of steps in thissignaling process… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Yu, O. (2016). GPCR and RhoA-Mediated Transcriptional Regulation. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/98d4j5cs

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yu, Olivia. “GPCR and RhoA-Mediated Transcriptional Regulation.” 2016. Thesis, University of California – San Diego. Accessed March 07, 2021. http://www.escholarship.org/uc/item/98d4j5cs.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yu, Olivia. “GPCR and RhoA-Mediated Transcriptional Regulation.” 2016. Web. 07 Mar 2021.

Vancouver:

Yu O. GPCR and RhoA-Mediated Transcriptional Regulation. [Internet] [Thesis]. University of California – San Diego; 2016. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/98d4j5cs.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yu O. GPCR and RhoA-Mediated Transcriptional Regulation. [Thesis]. University of California – San Diego; 2016. Available from: http://www.escholarship.org/uc/item/98d4j5cs

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Irvine

4. Gellner, Candice Ann. Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents.

Degree: Pharmacological Sciences with a concentration in Pharmacology Ph, 2017, University of California – Irvine

URL: http://www.escholarship.org/uc/item/18b1c9fc

► Cigarette smoking is the leading preventable cause of death in the United States. Of those who smoke, 9 out of 10 report trying their first… (more)

▼ Cigarette smoking is the leading preventable cause of death in the United States. Of those who smoke, 9 out of 10 report trying their first cigarette before the age of 18. Although most people who initiate tobacco use are teenagers, animal models for studying tobacco dependence have traditionally focused on how adult animals initiate, withdrawal from and relapse to cigarette smoking. Furthermore, cigarette smoke contains more than 7,000 constituents, including nicotine, yet pre-clinical research has focused on nicotine alone. Our lab began studying these constituents by creating cigarette smoke extract, CSE, a solution which contains the aqueous constituents present in cigarette smoke. Previous work from our lab found that CSE is more potent than nicotine alone and can enhance stress-induced reinstatement in adult male rats. In order to understand how the presence of tobacco smoke constituents may affect adolescents, I investigated the role of these constituents in models of smoking initiation and relapse. I found that the tobacco smoke constituents did not influence adolescent or adult acquisition of self-administration. Adolescents self-administered more low-dose nicotine than adults when their increased non-specific responding was corrected for. During reinstatement of drug seeking, I found that CSE enhanced stress- + cue-induced reinstatement of drug-seeking behavior with no effect of age. To investigate the role of tobacco smoke constituents on attenuation of adolescent self-administration, a novel smoking cessation pharmacotherapy, AT-1001, which is a selective α3β4 nAChR functional antagonist, was used. AT-1001 attenuated both CSE and nicotine self-administration in adolescent rats to a similar degree. My results suggest that both age and the presence of tobacco smoke constituents are important factors in establishing a proper model of tobacco dependence. Furthermore, my findings provide novel insights on adolescent initiation and relapse and offer an exciting potential for the development of a new tobacco dependence animal model that could help create innovative therapeutics to curb the addiction faced by many.

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Gellner, C. A. (2017). Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/18b1c9fc

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gellner, Candice Ann. “Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents.” 2017. Thesis, University of California – Irvine. Accessed March 07, 2021. http://www.escholarship.org/uc/item/18b1c9fc.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gellner, Candice Ann. “Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents.” 2017. Web. 07 Mar 2021.

Vancouver:

Gellner CA. Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents. [Internet] [Thesis]. University of California – Irvine; 2017. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/18b1c9fc.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gellner CA. Establishing a Proper Model of Tobacco Dependence: Influence of Age and Tobacco Smoke Constituents. [Thesis]. University of California – Irvine; 2017. Available from: http://www.escholarship.org/uc/item/18b1c9fc

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

UCLA

5. Thosani, Niyati Mehta. ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function.

Degree: Molecular and Medical Pharmacology, 2015, UCLA

URL: http://www.escholarship.org/uc/item/8kd0v8cm

► Objective: We previously reported that Hemopexin (Hx), an acute phase protein and a heme scavenger, is significantly increased and associated with proinflammatory HDL under atherogenic… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Thosani, N. M. (2015). ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/8kd0v8cm

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Thosani, Niyati Mehta. “ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function.” 2015. Thesis, UCLA. Accessed March 07, 2021. http://www.escholarship.org/uc/item/8kd0v8cm.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Thosani, Niyati Mehta. “ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function.” 2015. Web. 07 Mar 2021.

Vancouver:

Thosani NM. ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function. [Internet] [Thesis]. UCLA; 2015. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/8kd0v8cm.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Thosani NM. ApoE-/- Mice Lacking Hemopexin Develop Increased Atherosclerosis via Mechanisms That Include Oxidative Stress and Altered Macrophage Function. [Thesis]. UCLA; 2015. Available from: http://www.escholarship.org/uc/item/8kd0v8cm

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Irvine

6. Park, John. Mechanisms of Thrombospondin-4 in Pain Modulation.

Degree: Pharmacology and Toxicology, 2014, University of California – Irvine

URL: http://www.escholarship.org/uc/item/2496030f

► Upregulation of the thrombospondin-4 (TSP4) or calcium channel alpha-2-delta-1 subunit (Cava2d1) in the dorsal spinal cord and dorsal root ganglia plays a causal role in… (more)

▼ Upregulation of the thrombospondin-4 (TSP4) or calcium channel alpha-2-delta-1 subunit (Cava2d1) in the dorsal spinal cord and dorsal root ganglia plays a causal role in neuropathic pain development through an unidentified mechanism. TSP4 blockade either by antibodies or inactivation of the TSP4 gene prevents development of chronic pain states. Intrathecal injection of TSP4 proteins into naive rats can cause dorsal horn neuron hyperexcitability and allodynia, which are blocked by the Cava2d1 ligand gabapentin. These findings suggest that TSP4 and Cava2d1 may interact together in mediating pain processing. Here, I show that TSP4 binding to Cava2d1 is detectable in the same immunocomplexes from rodent spinal cords and in solid-phase binding. SPOT Peptide array analysis and in vitro binding of TSP4 recombinant truncation proteins to Cava2d1 reveal multiple binding sites within the TSP4 Epidermal Growth Factor-like domains (EGF-like) and coil-coil domain. Functionally, lumbar intrathecal injection of EGF-like domain proteins is sufficient to induce behavioral hypersensitivity. Selective ablation of Cava2d1 from Nav1.8-positive sensory neurons abolishes EGF-like domain induced thermal hyperalgesia, but not tactile allodynia. A 15-mer TSP4 peptide from the EGF-like domains can block both Cava2d1- and TSP4-induced behavioral hypersensitivity, presumably by disrupting the interaction between TSP4 and Cava2d1. My data suggest that the EGF-like domains of TSP4 interact with Cava2d1 to induce chronic pain states in a modality specific manner. Emerging data also suggest that Cava2d1 and TSP4 interact to induce synapse formation. To determine if maladaptive changes in synapses correlate with neuropathic pain states in a nerve injury model with injury-induced upregulation of TSP4 and Cava2d1, I examined synapse numbers at ultrastructure level in superficial dorsal horn of rats after trigeminal nerve injury. I found a significant increase in both excitatory and inhibitory synapses within lamina I and II of the superficial dorsal horn, respectively, and a decrease in mean synaptic length, a marker for synapse strength, of inhibitory interneurons mainly in lamina I of the injury side. Together, it is likely that injury-induced TSP4/Cava2d1 contribute to the development of chronic pain states after nerve injury through a mechanism involving dysregulation of excitatory and inhibitory synapses in the superficial dorsal horn.

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Park, J. (2014). Mechanisms of Thrombospondin-4 in Pain Modulation. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/2496030f

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Park, John. “Mechanisms of Thrombospondin-4 in Pain Modulation.” 2014. Thesis, University of California – Irvine. Accessed March 07, 2021. http://www.escholarship.org/uc/item/2496030f.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Park, John. “Mechanisms of Thrombospondin-4 in Pain Modulation.” 2014. Web. 07 Mar 2021.

Vancouver:

Park J. Mechanisms of Thrombospondin-4 in Pain Modulation. [Internet] [Thesis]. University of California – Irvine; 2014. [cited 2021 Mar 07]. Available from: http://www.escholarship.org/uc/item/2496030f.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Park J. Mechanisms of Thrombospondin-4 in Pain Modulation. [Thesis]. University of California – Irvine; 2014. Available from: http://www.escholarship.org/uc/item/2496030f

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Temple University

7. Fang, Pu. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.

Degree: PhD, 2012, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,223888

►

Pharmacology

Homocysteine (Hcy) is a thiol amino acid formed upon methionine de - methylation. A number of studies have revealed an association between hyperhomocysteinemia (HHcy),… (more)

▼

Pharmacology

Homocysteine (Hcy) is a thiol amino acid formed upon methionine de - methylation. A number of studies have revealed an association between hyperhomocysteinemia (HHcy), in which plasma Hcy levels exceed 15 µM, and diabetic atherosclerosis [1]. Despite these associations, the mechanisms underlying HHcy - associated diabetic atherosclerosis have not been clearly defined. This study assessed the effect of HHcy on diabetic atherosclerosis and its underlying mechanisms. We established a mouse model with a combination of three metabolic disorders, including HHcy (to mimic human HHcy), hyperglycemic (to mimic type 1 diabetes) and dyslipidemia (to exacerbate ApoE-/- mouse's susceptibility to atherosclerosis). In this mouse model, severe HHcy was developed due to mouse Cbs deficiency (mean plasma Hcy 182 µM) in a noval HHcy mouse model (Tg-hCBS Cbs ApoE-/-) generated by our collaborator [2]. Hyperglycemia was developed by 50 mg/kg streptozotocin (STZ) consecutive injection for 5 days (mean blood glucose 397 mg / dL). Dyslipedimia was introduced by high fat (HF, 21.0 % by weight) diet to accelerate aortic lesion formation in the Tg-hCBS Cbs ApoE-/- mice. An inducible human CBS (hCBS) transgene (Tg) was introduced to circumvent the neonatal lethality due to the mouse Cbs deficiency (Tg-hCBS Cbs-/- ApoE-/- mice). A zinc supplement in water could induce hCBS transgene expression and reverse Hcy level (reduced plasma Hcy from 182 µM to 5 µM, p < 0.001). Severe HHcy aggravated metabolic abnormalities, including increased urine secretion (from 8.35 ± 6.81 g/d/mouse in hyperglycemia only mice to 21.14 ± 5.95 g / d / mouse in hyperglycemic HHcy mice, p=0.042), increased water consumption (from 27.28 ± 9.46 g / d / mouse to 44.20 ± 4.66 g / d / mouse, p = 0.026), increased blood glucose level (from 443.20 ± 107.82 mg / dL to 614.27 ± 199.36 mg/dL, p = 0.031), increased heart weight (from 0.08 ± 0.02 g / cm to 0.11 ± 0.03 g / cm, p = 0.031) (data not shown) and decreased body weight (from -0.05 ± 0.92 g / 2 weeks / mouse to -1.78 ± 2.38 g / 2 weeks / mouse, p = 0.017). Hcy-lowering by zinc water reversed HHcy - induced hyperglycemia (from 614.27 ± 199.36 mg / dL to 440.20 ± 134.37 mg / dL, p = 0.032), increased urine secretion (from 21.14 ± 5.95 g / d / mouse to 0.90 ± 1.24 g / d / mouse, p = 0.042), and increased water consumption (from 44.20 ± 4.66 g / d / mouse to 6.08 ± 1.84 g / d / mouse, p = 0.008) in hyperglycemic mice. Increased atherosclerotic lesions were also found in the aortic roots of hyperglycemic HHcy mice (from 30.38 ± 14.34 % of the lumen area to 48.18 ± 12.07 %, p = 0.040). Increased accumulation of monocytes (MCs) and inflammatory MCs were found in atherosclerotic lesions of hyperglycemic HHcy mice. By sequential double immune - fluorescence staining with monoclonal antibodies (mAbs) anti MOMA - 2 (MC / macrophage [MØ] marker) and anti - Ly6C (inflammatory MC marker), we found that hyperglycemic HHcy mice had the largest area and percentage of MC / MØ (MOMA - 2+), and the largest area and percentage…

Advisors/Committee Members: Wang, Hong;, Yang, Xiao-Feng, Merali, Salim, Autieri, Michael V., Ashby, Barrie, Kruger, Warren D.;.

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fang, P. (2012). HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,223888

Chicago Manual of Style (16^th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Doctoral Dissertation, Temple University. Accessed March 07, 2021. http://digital.library.temple.edu/u?/p245801coll10,223888.

MLA Handbook (7^th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Web. 07 Mar 2021.

Vancouver:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2021 Mar 07]. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888.

Council of Science Editors:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888

Temple University

8. Pansuria, Meghanaben. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.

Degree: PhD, 2013, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,228447

►

Pharmacology

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease (CVD). Both HHcy and insulin resistance (IR) are associated with atherosclerotic CVD. Recent studies… (more)

▼

Pharmacology

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease (CVD). Both HHcy and insulin resistance (IR) are associated with atherosclerotic CVD. Recent studies have confirmed that insulin is not only a principle regulator of glucose homeostasis but also an important vasoactive hormone involved in the modulation of vascular tone. Epidemiological studies and animal studies have demonstrated the positive correlation of HHcy with IR and diabetes. Nevertheless, the effect and mechanism of HHcy on endothelial insulin signaling and insulin resistance has not been studied. In this study, we investigated the role and mechanism of HHcy on endothelial IR in vivo using transgenic mouse model of HHcy (Tg-hCBS Cbs -/- mice, plasma Hcy levels of 102.6 ± 9.1µmol/L) and in vitro using human aortic endothelial cells (HAEC). Using bioinformatics approach, we found tissue differential expression of Insulin/PI3K pathway genes in human and mouse. Furthermore, we measured tissue Hcy, S-adenosyl methionine (SAM), S-adenosyl homocysteine (SAH) levels in Tg-hCBS Cbs +/+ mice and examined correlation of insulin signaling genes with tissue Hcy, SAH levels and SAM/SAH ratio. We found negative correlation of Insulin/PI3K signaling genes with Hcy and SAH levels and positive correlation of Insulin/PI3K signaling genes with SAM/SAH ratio. These results led us to hypothesize that HHcy might negatively regulate insulin signaling and further contributes to IR. We found that HHcy impaired glucose metabolism (p<0.01 vs controls [CT]) and insulin sensitivity (p<0.05 vs CT) in Tg-hCBS Cbs -/- mice compared to their littermate controls (Tg-hCBS Cbs -/+ or +/+ mice). Furthermore, HHcy impaired insulin-induced vasorelaxation (31% vs CT, p<0.05) and endothelium-dependent relaxation (26% vs CT, p<0.05) in Tg-hCBS Cbs -/- mouse mesenteric arterioles. HHcy did not affect endothelium-independent relaxation and potassium chloride (KCl) & phenylephrine (PE)-induced contraction responses. Moreover, we found that HHcy significantly inhibited insulin-stimulated Akt and eNOS phosphorylation and activation in HAEC, mesenteric arterial tree, and in aorta. Pre-treatment of mesenteric arterioles with Wortmanin (PI3K inhibitor) and L-NAME (Nitric oxide synthase inhibitor) significantly inhibited insulin-induced vasorelaxation in controls (p<0.05 vs vehicle pre-treatment) but not in Tg-hCBS Cbs -/- mice, suggesting that HHcy impairs insulin-induced PI3K/Akt/eNOS signaling pathway. Moreover, we found that HHcy augmented insulin-induced MAPK pathway in HAEC, mesenteric arteries, and in aorta. In addition, pre-treatment of mesenteric arterioles with MEK inhibitor (PD98059) and endothelin-1A receptor blocker (BQ123) significantly improved (p<0.05 vs vehicle pre-treatment) insulin-induced vasorelaxation in Tg-hCBS Cbs -/- mice. Further analysis of upstream insulin signaling genes show that HHcy downregulated insulin receptor substrates (IRS) 1/2 mRNAs and protein expression but did not affect insulin receptor mRNA…

Advisors/Committee Members: Wang, Hong;, Yang, Xiao-Feng, Ashby, Barrie, Scalia, Rosario, Liu, Ming-Lin, Song, Wenchao;.

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pansuria, M. (2013). EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,228447

Chicago Manual of Style (16^th Edition):

Pansuria, Meghanaben. “EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.” 2013. Doctoral Dissertation, Temple University. Accessed March 07, 2021. http://digital.library.temple.edu/u?/p245801coll10,228447.

MLA Handbook (7^th Edition):

Pansuria, Meghanaben. “EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.” 2013. Web. 07 Mar 2021.

Vancouver:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2021 Mar 07]. Available from: http://digital.library.temple.edu/u?/p245801coll10,228447.

Council of Science Editors:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,228447

Stellenbosch University

9. Fasinu, Pius Sedowhe. In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential.

Degree: PhD, Medicine, 2013, Stellenbosch University

URL: http://hdl.handle.net/10019.1/85850

► ENGLISH ABSTRACT: Introduction Earlier studies have shown the popularity of herbal products among people as traditional, complementary or alternative medication. One of the major clinical… (more)

▼ ENGLISH ABSTRACT: Introduction Earlier studies have shown the popularity of herbal products among people as traditional, complementary or alternative medication. One of the major clinical risks in the concomitant administration of herbal products and prescription medicine is pharmacokinetic herb-drug interaction (HDI). This is brought about by the ability of phytochemicals to inhibit or induce the activity of metabolic enzymes and transport proteins. The aim of this study was to investigate the potential of the crude extracts of popular medicinal herbs used in South Africa to inhibit major cytochrome P450 (CYP) enzymes and transport proteins through in vitro assessment. Methods Medicinal herbs were obtained from traditional medical practitioners and 15 were selected for this study. The selected herbal products were extracted and incubated with human liver microsomes to monitor the following reactions as markers for the metabolic activities of the respective CYP: phenacetin O-deethylation (CYP1A2), diclofenac 4‟-hydroxylation (CYP2C9), S-mephenytoin 4‟- hydroxylation (CYP2C19) and testosterone 6β-hydroxylation (CYP3A4). In addition, the influence of Lessertia frutescens (formerly Sutherlandia frutescens) and Hypoxis hemerocallidea was investigated on more isozymes: coumarin 7-hydroxylation (CYP2A6), bupropion hydroxylation (CYP2B6), paclitaxel 6α-hydroxylation (CYP2C8), bufuralol 1‟-hydroxylation (CYP2D6), chlorzoxazone 6- hydroxylation (CYP2E1) and midazolam 1‟-hydroxylation (CYP3A4/5). The generation of the CYPspecific substrates/metabolites were monitored and quantified with the aid of LC-MS/MS. The metabolic clearance of midazolam using cryopreserved hepatocytes was monitored in the presence of Lessertia frutescens and Hypoxis hemerocallidea. The potential of both to inhibit human ATP-binding cassette (ABC) transporter activity was assessed using recombinant MDCKII and LLC-PK1 cells overexpressing human breast cancer resistant protein (BCRP) and human P-glycoprotein (P-gp), respectively. Similarly, the potential for interactions with human organic anion transporting polypeptide (OATP1B1 and OATP1B3) was assessed using recombinant HEK293 cells over-expressing OATP1B1 and OATP1B3, respectively. Results Bowiea volubilis, Kedrostis Africana, Chenopodium album, Lessertia frutescens (methanolic extract), Hypoxis hemerocallidea, Spirostachys africana and Lessertia frutescens (aqueous extract), in ascending order of potency demonstrated strong inhibition of CYP1A2 activity (IC50 = 1-100 g/mL). Similarly, Emex australis, Alepidea amatymbica, Pachycarpus concolor, Lessertia frutescens, Capparis sepiaria, Kedrostis africana and Pentanisia prunelloides inhibited CYP2C9 with IC50 less than 100 g/mL. The following demonstrated strong inhibition of CYP2C19 with IC50 values less than 100 g/mL: Acacia karroo, Capparis sepiaria, Chenopodium album, Pachycarpus concolor, Ranunculus multifidus, Lessertia frutescens and Zantedeschia aethiopica. CYP3A4 was inhibited by Lessertia frutescens, Hypoxis… Advisors/Committee Members: Rosenkranz, Bernd, Bouic, Patrick J., Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Medicine. Division of Clinical Pharmacology..

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fasinu, P. S. (2013). In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential. (Doctoral Dissertation). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/85850

Chicago Manual of Style (16^th Edition):

Fasinu, Pius Sedowhe. “In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential.” 2013. Doctoral Dissertation, Stellenbosch University. Accessed March 07, 2021. http://hdl.handle.net/10019.1/85850.

MLA Handbook (7^th Edition):

Fasinu, Pius Sedowhe. “In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential.” 2013. Web. 07 Mar 2021.

Vancouver:

Fasinu PS. In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential. [Internet] [Doctoral dissertation]. Stellenbosch University; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10019.1/85850.

Council of Science Editors:

Fasinu PS. In vitro assessment of some traditional medications used in South Africa for pharmacokinetics drug interaction potential. [Doctoral Dissertation]. Stellenbosch University; 2013. Available from: http://hdl.handle.net/10019.1/85850

Stellenbosch University

10. De Kock, Lizanne. Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment.

Degree: MSc in Medical Science, Medicine, 2013, Stellenbosch University

URL: http://hdl.handle.net/10019.1/85726

► ENGLISH ABSTRACT: Background: Para-aminosalicylic acid (PAS) is one of the first effective anti-tuberculosis agents and has become one of the principal second-line drugs to treat… (more)

▼ ENGLISH ABSTRACT: Background: Para-aminosalicylic acid (PAS) is one of the first effective anti-tuberculosis agents and has become one of the principal second-line drugs to treat patients with an extended resistance spectrum. Despite being one of the oldest anti-tuberculosis drugs, little data is available regarding its pharmacokinetics, drug interactions, genetic factors and dosing regimens, especially for the relative new granular slow release PAS (GSR-PAS) preparation. Objectives The aim of the study was to investigate the pharmacokinetics, tolerability and safety of a single 8 g once- or 4 g twice-daily GSR-PAS dose in a multidrug- or extensively drug resistant tuberculosis (M/XDR-TB) population, in which some subjects were also co-infected with the human immunodeficiency virus (HIV). An additional objective was to investigate the potential covariates (i.e. genetic factors and drug interactions) that can alter the pharmacokinetics of PAS. Study design and methodology A randomised, two-period, open-label cross-over study was conducted in 32 adults (≥18 years old) with M/XDR-TB admitted at Brooklyn Chest Hospital, Cape Town, South Africa and treated for drug resistant tuberculosis with a multidrug regimen containing GSR-PAS. The subjects were randomised to follow a single 8 g once-daily GSR-PAS regimen or a 4 g twice-daily GSR-PAS regimen for 8 days. On the eighth day blood samples were obtained at 0, 1, 2, 3, 4, 6, 8, 12 and 24 hours. After the 24-hour sample (Day 9) the regimens were crossed-over. The tolerability and safety of the two regimens were determined using Visual Analogue Scales and interviews. PAS plasma concentrations were determined by a developed HPLC-MS/MS method. N-acetyltransferase (NAT1 and NAT2) genotyping was performed. The data of this study together with unpublished data of a previous study in a very similar population were used in a pharmacometric analysis to determine the PK parameters and any subject covariates. Results and Discussion In comparison to the 4 g twice-daily GSR-PAS dose, the single 8 g once-daily GSR-PAS dose generated a pharmacokinetic profile with a significantly higher maximum concentration (Cmax), concentration at 12 hours (C12) and area under the curve 0 to 12 hours (AUC12). The concentrations of all subjects on the twice-daily regimen were maintained above a minimum inhibitory concentration (MIC) throughout a 12-hour interval, while the single 8 g dose was able to sustain the PAS plasma concentrations above the MIC in 18 out of 29 subjects (62.1%) for the entire 24-hour dosing interval. Both regimens were reasonably well tolerated but most subjects preferred the twice-daily dosing. The clearance of PAS was increased by 45% in HIV positive subjects prescribed antiretroviral treatment (ART), possibly due to interaction with efavirenz (EFV). No significant associations were found for any of the individual NAT1 or NAT2 genotypes, but a difference between mean concentrations of the different genotypic groups was reported. Conclusions The 8 g once-daily dose has the… Advisors/Committee Members: Rosenkranz, B., Diacon, A. H., Stellenbosch University. Faculty of Medicine and Health Sciences. Dept. of Medicine. Clinical Pharmacology..

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

De Kock, L. (2013). Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment. (Masters Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/85726

Chicago Manual of Style (16^th Edition):

De Kock, Lizanne. “Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment.” 2013. Masters Thesis, Stellenbosch University. Accessed March 07, 2021. http://hdl.handle.net/10019.1/85726.

MLA Handbook (7^th Edition):

De Kock, Lizanne. “Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment.” 2013. Web. 07 Mar 2021.

Vancouver:

De Kock L. Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment. [Internet] [Masters thesis]. Stellenbosch University; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/10019.1/85726.

Council of Science Editors:

De Kock L. Pharmacokinetics of twice-daily versus once-daily dosing with granular slow-release para-aminosalicylic acid in adults on second-line anti-tuberculosis and antiretroviral treatment. [Masters Thesis]. Stellenbosch University; 2013. Available from: http://hdl.handle.net/10019.1/85726

11. Jackson, Fred Vernon. Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei.

Degree: Department of Molecular Pharmacology, Physiology and Biotechnology, 2017, Brown University

URL: https://repository.library.brown.edu/studio/item/bdr:733364/

► Abstract of “Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei” by Fred V. Jackson, Ph.D., Brown University, May… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Jackson, F. V. (2017). Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei. (Thesis). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:733364/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Jackson, Fred Vernon. “Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei.” 2017. Thesis, Brown University. Accessed March 07, 2021. https://repository.library.brown.edu/studio/item/bdr:733364/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Jackson, Fred Vernon. “Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei.” 2017. Web. 07 Mar 2021.

Vancouver:

Jackson FV. Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei. [Internet] [Thesis]. Brown University; 2017. [cited 2021 Mar 07]. Available from: https://repository.library.brown.edu/studio/item/bdr:733364/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jackson FV. Nutrient and Drought Responses on the Secondary Metabolite Production in the Medicinal Plant Mondia whytei. [Thesis]. Brown University; 2017. Available from: https://repository.library.brown.edu/studio/item/bdr:733364/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University

12. Mustaly, Hatim Mustafa. Identification of small molecule modulators of the Hippo tumor suppressor pathway.

Degree: MS, Medical Sciences, 2015, Boston University

URL: http://hdl.handle.net/2144/16121

► The Hippo signaling pathway, originally identified in Drosophila melanogaster and later shown to be conserved in mammals, is essential in regulating organ size and maintaining… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Mustaly, H. M. (2015). Identification of small molecule modulators of the Hippo tumor suppressor pathway. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16121

Chicago Manual of Style (16^th Edition):

Mustaly, Hatim Mustafa. “Identification of small molecule modulators of the Hippo tumor suppressor pathway.” 2015. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/16121.

MLA Handbook (7^th Edition):

Mustaly, Hatim Mustafa. “Identification of small molecule modulators of the Hippo tumor suppressor pathway.” 2015. Web. 07 Mar 2021.

Vancouver:

Mustaly HM. Identification of small molecule modulators of the Hippo tumor suppressor pathway. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/16121.

Council of Science Editors:

Mustaly HM. Identification of small molecule modulators of the Hippo tumor suppressor pathway. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16121

Boston University

13. Kim, Andrew. Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption.

Degree: 2015, Boston University

URL: http://hdl.handle.net/2144/16268

► Alcoholism results from an interaction between genetic and environmental factors. However, the neurobiological mechanisms mediating the propensity to consume excessive amounts of alcohol are still… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Kim, A. (2015). Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption. (Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/16268

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kim, Andrew. “Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption.” 2015. Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/16268.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kim, Andrew. “Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption.” 2015. Web. 07 Mar 2021.

Vancouver:

Kim A. Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption. [Internet] [Thesis]. Boston University; 2015. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/16268.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kim A. Pituitary adenylate cyclase-activating polypeptide regulates excessive alcohol consumption. [Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/16268

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

14. Dees, Sundee. Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer.

Degree: 2020, University of the Sciences in Philadelphia

URL: http://pqdtopen.proquest.com/#viewpdf?dispub=27671415

► Being the most aggressive subtype of breast cancer (BCa), triple negative breast cancer (TNBC) is defined by its heightened metastatic potential and is associated with… (more)

▼ Being the most aggressive subtype of breast cancer (BCa), triple negative breast cancer (TNBC) is defined by its heightened metastatic potential and is associated with poor survival rates. Women diagnosed with TNBC do not respond to traditional targeted therapies because their tumors lack the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Due to undesirable side effects resulting from chemotherapeutics, the development of targeted treatment options for the TNBC patient population is warranted. Signal transducer and activator of transcription 3 (STAT3) has emerged as a promising therapeutic target in BCa and targeting this transcription factor has proven to be a viable approach to halt cancer growth in vitro and in vivo. Extensive research efforts are ongoing to bring STAT3 inhibitors to market for the treatment of TNBC. The FDA-approved antipsychotic drug pimozide has demonstrated efficacy as a STAT3 inhibitor in several cancers, however, its role on this pathway in TNBC remains unexplored. Due to intrinsic heterogeneity present among TNBCs and because a “one size fits all” approach cannot be applied to this aggressive cancer, we hypothesized that STAT3 could be a novel biomarker predictive of response to pimozide therapy in TNBC. Our research utilized human cell lines representative of four TNBC molecular subtypes: basal-like 1, basal-like 2, mesenchymal-like, and mesenchymal stem-like. Herein, we report that STAT3 phosphorylation on tyrosine residue 705 (Tyr705) dictated the ability of pimozide to significantly reduce the invasion and migration of TNBC subtypes. Mechanistically, downregulation of downstream STAT3 transcriptional targets implicated in invasion and migration, such as matrix metalloproteinase-9 (MMP-9) or vimentin, was observed upon inhibition of phosphorylated STAT3 (Tyr705) by pimozide treatment. Our results identify phosphorylated STAT3 (Tyr705) to be a promising and novel biomarker to guide pimozide therapy.

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Dees, S. (2020). Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer. (Thesis). University of the Sciences in Philadelphia. Retrieved from http://pqdtopen.proquest.com/#viewpdf?dispub=27671415

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Dees, Sundee. “Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer.” 2020. Thesis, University of the Sciences in Philadelphia. Accessed March 07, 2021. http://pqdtopen.proquest.com/#viewpdf?dispub=27671415.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Dees, Sundee. “Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer.” 2020. Web. 07 Mar 2021.

Vancouver:

Dees S. Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer. [Internet] [Thesis]. University of the Sciences in Philadelphia; 2020. [cited 2021 Mar 07]. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=27671415.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Dees S. Phosphorylated STAT3 (Tyr705) as a Biomarker of Response to Pimozide Treatment in Triple Negative Breast Cancer. [Thesis]. University of the Sciences in Philadelphia; 2020. Available from: http://pqdtopen.proquest.com/#viewpdf?dispub=27671415

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

West Virginia University

15. Fishback, James A. New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands.

Degree: PhD, Pharmaceutical Sciences, 2011, West Virginia University

URL: https://doi.org/10.33915/etd.4712 ; https://researchrepository.wvu.edu/etd/4712

► Sigma receptors represent a promising drug development target for a number of therapeutic indications including cancer, depression, psychostimulant abuse and stroke. To date, two subtypes… (more)

▼ Sigma receptors represent a promising drug development target for a number of therapeutic indications including cancer, depression, psychostimulant abuse and stroke. To date, two subtypes of sigma receptors have been identified; sigma1 and sigma2. Their respective roles in normal physiology and in disease processes are a subject of ongoing studies. Consequently, the discovery and development of subtype specific agonist and antagonist ligands remains a key research goal. To date, no in vitro functional assay suitable for routine screening of putative sigma ligands has been reported. As a result, radioligand binding assays are used as a primary screen. Therefore, to support the critical role of receptor binding assays, a new sigma1 selective radioligand, [3H]-SN56, was characterized, and efforts were undertaken to develop medium throughput methods for binding affinity determinations for both sigma receptor subtypes. To fill the unmet need for an in vitro functional assay for sigma1 ligands, preliminary studies were performed to develop an immunological assay based on the ligand sensitive interaction of sigma1 and binding immunoglobulin protein (BiP). The results of the studies with [3H]SN56 show that it possesses high affinity and selectivity for sigma1 receptors and offers considerable advantages over the currently used radioligand, [3H](+)- pentazocine. Competition binding studies with established sigma ligands assayed in rat brain homogenates labeled with [3H]SN56 or [ 3H](+)-pentazocine yielded comparable Ki values, indicating that the two radioligands bind the same site. Saturation studies revealed similar Bmax values for [3H]SN56 and [3H](+)-pentazocine, further supporting the notion that both ligands bind specifically to the site identified as the sigma1 receptor. Conventional radioligand binding studies for sigma receptors utilize a "cell harvester." Newer medium and high throughput technologies exist that have been applied to the analysis of numerous classical receptors. 96-well filtration and scintillation proximity assay (SPA) were evaluated for the analysis of sigma receptor ligand binding. Adaptation of the conventional binding assay to the higher throughput methods required the use of rat liver membranes because sigma receptor densities were too low in rat brain membranes to support reliable filtration in the 96-well format or use with SPA. Analysis of a series of reference compounds by 96-well filtration yielded binding affinities that correlated with values measured using the conventional method, for both sigma receptor subtypes. Following validation with the reference compounds, the 96-well filtration procedure was successfully used to determine Ki values for sigma receptors for a novel series of 2(3)-benzothiazolones. Studies with SPA demonstrated that this technique also yields results that are equivalent to the conventional method, but the cost of beads is prohibitively high with currently available radioligands used in conjunction with tissue derived membranes; this cost could potentially be… Advisors/Committee Members: Rae R Matsumoto.

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fishback, J. A. (2011). New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands. (Doctoral Dissertation). West Virginia University. Retrieved from https://doi.org/10.33915/etd.4712 ; https://researchrepository.wvu.edu/etd/4712

Chicago Manual of Style (16^th Edition):

Fishback, James A. “New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands.” 2011. Doctoral Dissertation, West Virginia University. Accessed March 07, 2021. https://doi.org/10.33915/etd.4712 ; https://researchrepository.wvu.edu/etd/4712.

MLA Handbook (7^th Edition):

Fishback, James A. “New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands.” 2011. Web. 07 Mar 2021.

Vancouver:

Fishback JA. New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands. [Internet] [Doctoral dissertation]. West Virginia University; 2011. [cited 2021 Mar 07]. Available from: https://doi.org/10.33915/etd.4712 ; https://researchrepository.wvu.edu/etd/4712.

Council of Science Editors:

Fishback JA. New methodologies for in vitro analysis of binding and functional activity of sigma receptor ligands. [Doctoral Dissertation]. West Virginia University; 2011. Available from: https://doi.org/10.33915/etd.4712 ; https://researchrepository.wvu.edu/etd/4712

Wayne State University

16. Shen, Min. Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins.

Degree: PhD, Pharmacology, 2013, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/796

► Although considerable progress has been achieved in the field of cancer therapeutics, primary or acquired drug resistance remains a fundamental cause of therapeutic failure… (more)

▼ Although considerable progress has been achieved in the field of cancer therapeutics, primary or acquired drug resistance remains a fundamental cause of therapeutic failure in cancer therapy. Among different mechanisms characterized that are responsible for tumor drug resistance, there is increasing evidence suggesting that dysregulation of gene expression, especially oncogene or tumor suppressor gene expression, at either gene transcription or protein synthesis level, can contribute to the drug-resistant phenotype. AMP-activated protein kinase (AMPK) is a well-known major cellular energy sensor, which negatively regulates metabolic pathways such as protein synthesis, fatty acid oxidation and glucose consumption. Activation of AMPK may suppress metabolic activities that are in favor of assisting tumor cell growth and resistance to various anti-tumor drugs. Along this line, I hypothesized that activation of AMPK signaling could help overcoming tumor drug resistance. The data presented in this dissertation strongly support this hypothesis. The hypothesis was investigated in two different types of cancers with resistance to two different types of drugs. The first model system I used to test my hypothesis is prostate cancer cell models. By using androgen-dependent, androgen receptor (AR)-positive LNCaP cell line and its androgen-independent, AR-positive derivative C4-2B cell line, I found that both cell lines responded to pharmacological AMPK activator metformin, regardless of their androgen dependency. Activation of AMPK by metformin caused AR protein level decrease through suppression of AR mRNA expression and promotion of AR protein degradation. On the other hand, I found that AR is an inhibitor of AMPK signaling-mediated growth suppression and cell death in prostate cancer cells. These findings suggest that combination of AR inhibition therapy with metformin or other AMPK activators may benefit the therapeutic outcome of AR-positive prostate cancer. The hypothesis has also been studied in multiple myeloma cell models in which paired parental bortezomib-sensitive multiple myeloma cells and their bortezomib-resistant counterparts generated by chronic drug exposure were used. In this study, I found that paired bortezomib-sensitive and -resistant multiple myeloma cells were about equally sensitive to AMPK activators metformin and AICAR. Although carfilzomib is developed as next-generation proteasome inhibitor to overcome bortezomib resistance; the two bortezomib-resistant multiple myeloma cell lines tested in this study exhibited cross-resistance to carfilzomib. I also found that AMPK signaling is suppressed in bortezomib-resistant multiple myeloma cells and that the suppressed AMPK signaling can be elevated by challenging with an AMPK activator. Finally, I found that AMPK activators were able to overcome not only resistance to bortezomib but also cross-resistance to carfilzomib in bortezomib-resistant multiple myeloma cells. These findings support the further investigation of AMPK… Advisors/Committee Members: Q. Ping Dou.

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shen, M. (2013). Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/796

Chicago Manual of Style (16^th Edition):

Shen, Min. “Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins.” 2013. Doctoral Dissertation, Wayne State University. Accessed March 07, 2021. https://digitalcommons.wayne.edu/oa_dissertations/796.

MLA Handbook (7^th Edition):

Shen, Min. “Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins.” 2013. Web. 07 Mar 2021.

Vancouver:

Shen M. Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins. [Internet] [Doctoral dissertation]. Wayne State University; 2013. [cited 2021 Mar 07]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/796.

Council of Science Editors:

Shen M. Overcoming Tumor Drug Resistance By Activating Amp-Activated Protein Kinase And Destabilizing Oncoproteins. [Doctoral Dissertation]. Wayne State University; 2013. Available from: https://digitalcommons.wayne.edu/oa_dissertations/796

17. Ristic, Gorica. Deubiquitinases In Ubiquitin Homeostasis And Disease.

Degree: PhD, Pharmacology, 2017, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/1863

► Protein quality control (PQC) is indispensable for normal cellular functions, ensuring proteins are properly folded and removing those proteins that are functioning aberrantly. Perturbations… (more)

▼ Protein quality control (PQC) is indispensable for normal cellular functions, ensuring proteins are properly folded and removing those proteins that are functioning aberrantly. Perturbations in PQC can lead to various malignancies, neurodegeneration and neurological diseases. The Ubiquitin-Proteasome Pathway (UPP) is one important pathway in PQC, it relies on ubiquitination-dependent post-translational modification to selectively degrade misfolded or short-lived protein. Ubiquitination is reversed by the action of proteases known as deubiquitinating enzymes (DUBs). By hydrolyzing ubiquitin linkages, DUBs are responsible for cleaving and activating newly produced ubiquitin molecules, editing poly-Ub chains, removing ubiquitin from a substrate protein and recycling mono-Ub. Here, I investigated two proteins critically involved in the UPP: one that is important for normal cellular function (USP5), and another whose mutations cause neurodegeneration (ataxin-3). Ubiquitin Specific Protease 5 (USP5) is a member of the USP class of DUBs. Based on structural and in vitro results, it was long thought to function as a recycler of mono-Ub in the cell, by hydrolyzing unanchored poly-Ub chains. We studied the function of USP5 in vivo in Drosophila melanogaster. Knockdown of DmUSP5 in the whole fly results in death during developmental stages and in an increase in poly-Ub chains, but does not result in a depletion of mono-Ub in the fly, contrary to long-held opinion. Based on our data, lethality from USP5 knockdown is not due to depletion of mono-Ub, but likely resulted due to accumulation of unanchored poly-Ub chains and disruption of proteasomal degradation. Our results also suggest that USP5 has specific substrates. The other DUB investigated, ataxin-3, is the disease causing protein in the age-related, poly-glutamine (polyQ) dependent disease Spinocerebellar Ataxia Type-3 (SCA3). Through its different interacting partners, ataxin-3 is involved in protein quality control pathways. One such protein is the AAA ATPase Valosin Containing Protein (VCP). Ataxin-3 interacts directly with VCP through a VCP Binding Motif (VBM). Through biochemistry, Drosophila genetics and physiological assays, we showed that pathogenic ataxin-3 with a mutated VBM is markedly less toxic than its intact pathogenic counterpart. Mutating the VBM of ataxin-3 caused a delay in the aggregation of ataxin-3 in vivo, in various tissues tested. We propose that VCP acts as a nucleation center to increase local concentrations of ataxin-3 proteins and increase their likelihood of interacting and fibrilization. Our work suggest this interaction as a potential therapeutic target for SCA3. Advisors/Committee Members: Sokol V. Todi.

Subjects/Keywords: Pharmacology

10 more images…

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APA (6^th Edition):

Ristic, G. (2017). Deubiquitinases In Ubiquitin Homeostasis And Disease. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/1863

Chicago Manual of Style (16^th Edition):

Ristic, Gorica. “Deubiquitinases In Ubiquitin Homeostasis And Disease.” 2017. Doctoral Dissertation, Wayne State University. Accessed March 07, 2021. https://digitalcommons.wayne.edu/oa_dissertations/1863.

MLA Handbook (7^th Edition):

Ristic, Gorica. “Deubiquitinases In Ubiquitin Homeostasis And Disease.” 2017. Web. 07 Mar 2021.

Vancouver:

Ristic G. Deubiquitinases In Ubiquitin Homeostasis And Disease. [Internet] [Doctoral dissertation]. Wayne State University; 2017. [cited 2021 Mar 07]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1863.

Council of Science Editors:

Ristic G. Deubiquitinases In Ubiquitin Homeostasis And Disease. [Doctoral Dissertation]. Wayne State University; 2017. Available from: https://digitalcommons.wayne.edu/oa_dissertations/1863

Wayne State University

18. Baidwan, Sartaj S. Metformin, Glucotoxicity And Islet Dysfunction.

Degree: MS, Pharmaceutical Sciences, 2017, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_theses/548

► METFROMIN, GLUCOTOXICITY AND ISLET DYSFUNCTION by SARTAJ BAIDWAN MAY 2017 Advisor: Dr. Anjaneyulu Kowluru Major: Pharmaceutical Sciences Degree: Master of Science Glucotoxicity is the… (more)

▼ METFROMIN, GLUCOTOXICITY AND ISLET DYSFUNCTION by SARTAJ BAIDWAN MAY 2017 Advisor: Dr. Anjaneyulu Kowluru Major: Pharmaceutical Sciences Degree: Master of Science Glucotoxicity is the leading cause for β-cell dysfunction [e.g., defective glucose-stimulated insulin secretion] in Type 2 Diabetes [T2DM]. Recent studies from our lab have shown sustained Rac1 activation leading to the activation of downstream signaling steps including stress kinase [p53, p38MAPK] activation and mitochondrial dysregulation [caspase-3 activation] in pancreatic islet beta-cells exposed to glucotoxic [HG] conditions [20 mM; 24 hrs]. Metformin [MF] is an oral anti-diabetic drug that is being widely prescribed to T2DM. MF works by suppressing hepatic glucose production and increasing glucose uptake by the target tissues. However, potential beneficial effects of MF on pancreatic beta-cell dysfunction under HG conditions have not been studied to date. Therefore, in the current studies, we asked if MF [0-30 μM; clinically relevant concentrations] affords protective effects against HG-induced metabolic dysfunction of the pancreatic beta [INS-1 832/13] cells. Since recent studies from our laboratory have demonstrated activation of Rac1, a small G-protein, as an upstream signaling event to stress kinase activation, we asked if protective effects of MF may, in part, be due to inhibition of HG-induced Rac1 activation in INS-1 832/13 cells. Data from these studies have suggested nearly 40% inhibition in HG-induced Rac1 activation [3.43±0.57 fold over basal; n=4; p<0.05] by MF. Evidence is also presented to highlight novel roles for sustained activation of Rac1 in HG-induced expression of Cluster of Differentiation 36 [CD36], a fatty acid transporter protein, which is implicated in cell apoptosis. Western blot analysis indicated a significant increase in the phosphorylation of p38MAPK [2.31±0.21 fold over basal; n=5; p<0.05], JNK1/2 and phosphorylation of p53 [4.42±1.20 fold over basal; n=3; p<0.05] in INS-1 832/13 cells. MF [15µM] markedly attenuated HG-induced p38MAPK [74.8%], JNK 1 and p53 [55.7%] activation under these experimental conditions. Our data from Bax phosphorylation [an indicator of cell dysregulation] studies demonstrated an increase in the phosphorylation of two Bax isoforms [Baxα by 1.63± 0.04 fold over basal; n=3; p<0.05; and Baxβ by 1.32±0.11 over basal; n=3; p<0.05]. MF [30µM] attenuated the phosphorylation of only Baxα isoform [by 77.3%]. Lastly, our data also suggested that co-provision of MF significantly reduced [72.4%] HG-induced caspase-3 activation. Together, these findings suggest significant protection by MF against HG-induced metabolic defects [activation of Rac1-stress kinase-caspase-3 signaling module] in the islet beta-cell. Potential implications of these findings in the context of novel and direct regulation of islet β-cell function by metformin are discussed. Advisors/Committee Members: Anjaneyulu Kowluru.

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Baidwan, S. S. (2017). Metformin, Glucotoxicity And Islet Dysfunction. (Masters Thesis). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_theses/548

Chicago Manual of Style (16^th Edition):

Baidwan, Sartaj S. “Metformin, Glucotoxicity And Islet Dysfunction.” 2017. Masters Thesis, Wayne State University. Accessed March 07, 2021. https://digitalcommons.wayne.edu/oa_theses/548.

MLA Handbook (7^th Edition):

Baidwan, Sartaj S. “Metformin, Glucotoxicity And Islet Dysfunction.” 2017. Web. 07 Mar 2021.

Vancouver:

Baidwan SS. Metformin, Glucotoxicity And Islet Dysfunction. [Internet] [Masters thesis]. Wayne State University; 2017. [cited 2021 Mar 07]. Available from: https://digitalcommons.wayne.edu/oa_theses/548.

Council of Science Editors:

Baidwan SS. Metformin, Glucotoxicity And Islet Dysfunction. [Masters Thesis]. Wayne State University; 2017. Available from: https://digitalcommons.wayne.edu/oa_theses/548

University of Vermont

19. Mylie, Quentin. The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice.

Degree: MS, Pharmacology, 2018, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/902

► Recent studies have demonstrated that activation of the 5-HT4 receptors in the colonic mucosa can have healing and protective actions in experimental models of… (more)

▼ Recent studies have demonstrated that activation of the 5-HT4 receptors in the colonic mucosa can have healing and protective actions in experimental models of colitis. These actions include increased mucus secretion, increased epithelial proliferation, and enhanced epithelial migration. Since these studies involved chemically induced models of colitis, the current investigation was conducted to test whether a protective action of 5-HT4 receptor stimulation could be detected in Interleukin-10 knockout (IL-10 KO), which develop colitis spontaneously due to the absence of the anti-inflammatory cytokine, interleukin-10. Upon weaning, the IL-10 knockout mice were separated into two groups: an agonist group and a vehicle control group. The agonist group received 1 mg/kg tegaserod in a vehicle consisting of 0.9% saline each day by enema of dimethyl sulfoxide (DMSO) in saline each day, while the control group received daily enemas of vehicle over the course of 21 days. Several outcome measures were used to assess the effectiveness of the treatment. To evaluate the severity of colitis, disease activity index was monitored, and histologic damage was blindly scored. Administration of tegaserod by enema to the IL-10 KO mice had a significant protective effect on the treated mice. The disease activity index (DAI) of agonist treated mice was significantly better than that of vehicle treated mice over time (p<0.001; 2-way ANOVA). Mice treated with vehicle had a more significant decline in health over time versus the agonists, with more blood present in feces and a looser/diarrhea-like consistency in stool. The histological damage score (HDS) was also improved by 5-HT4 agonist treatment (p<0.05, t-test). Sections of vehicle treated colons showed significantly greater damage, including epithelial erosions, the presence of polymorphonuclear cells, and abnormal crypt architecture (cryptitis), than those treated with the 5-HT4 receptor agonist tegaserod. During the 21-day course of the current investigation, there was no difference in the survival data between the two groups. These data, when taken together, suggest that administration of the 5-HT4 receptor agonist tegaserod via enema to IL-10 KO mice has a greater healing and protective effect than seen in the IL-10 KO mice that received vehicle. We proposed to test the hypothesis that treatment of IL-10 knockout colitis with a 5-HT4 receptor agonist will attenuate the development of colitis and have healing and protective effects in the colons of the treated mice. Advisors/Committee Members: Gary Mawe.

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Mylie, Q. (2018). The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/902

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mylie, Quentin. “The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice.” 2018. Thesis, University of Vermont. Accessed March 07, 2021. https://scholarworks.uvm.edu/graddis/902.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mylie, Quentin. “The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice.” 2018. Web. 07 Mar 2021.

Vancouver:

Mylie Q. The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice. [Internet] [Thesis]. University of Vermont; 2018. [cited 2021 Mar 07]. Available from: https://scholarworks.uvm.edu/graddis/902.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mylie Q. The Effects Of 5-Ht4 Receptor Agonists On Interleukin-10 Knockout Mice. [Thesis]. University of Vermont; 2018. Available from: https://scholarworks.uvm.edu/graddis/902

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cape Town

20. Combrinck, Jill Michelle. The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum.

Degree: Image, Division of Clinical Pharmacology, 2016, University of Cape Town

URL: http://hdl.handle.net/11427/22760

► The malaria parasite detoxifies host red blood cell derived haem by conversion into the inert biocrystal haemozoin. Inhibiting this critical pathway is proposed to be… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Combrinck, J. M. (2016). The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum. (Thesis). University of Cape Town. Retrieved from http://hdl.handle.net/11427/22760

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Combrinck, Jill Michelle. “The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum.” 2016. Thesis, University of Cape Town. Accessed March 07, 2021. http://hdl.handle.net/11427/22760.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Combrinck, Jill Michelle. “The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum.” 2016. Web. 07 Mar 2021.

Vancouver:

Combrinck JM. The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum. [Internet] [Thesis]. University of Cape Town; 2016. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/11427/22760.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Combrinck JM. The role of haem in the mechanism of action of antimalarials in Plasmodium falciparum. [Thesis]. University of Cape Town; 2016. Available from: http://hdl.handle.net/11427/22760

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Cape Town

21. Gabriels, Gary Anthony. The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration.

Degree: Image, Division of Clinical Pharmacology, 2013, University of Cape Town

URL: http://hdl.handle.net/11427/3281

► Nutritional supplements are used by competitive and recreational athletes of all ages. As a consequence the supplement industry has grown to meet the increasing demand.… (more)

▼ Nutritional supplements are used by competitive and recreational athletes of all ages. As a consequence the supplement industry has grown to meet the increasing demand. The regulation of the supplement industry is unrefined, which increases the risk of the nutritional supplements being contaminated. Contamination may be intentional, where the companies “spike” their products with an ergogenic aid, or unintentional. A consequence of contamination is that an athlete may fail a drug test after ingesting a contaminated supplement or there may be negative health consequences. Without adequate legislation it is difficult to control the industry and reduce the risk of contamination in the supplement. Objectives: To investigate the industry associated with commercially available nutritional and traditional supplements. These are in the five specific areas; (i) to review the regulations and legislations, and labelling and claims associated with nutritional products in the USA, European Union and South Africa, (ii) to assess the labelling and claims information on nutritional supplement products imported into and manufactured or assembled in South Africa, (iii) to assess using a survey questionnaire the container labelling and other sources of information that assist consumers of nutritional products in their purchasing decisions, (iv) to assess traditional commercial supplements for contamination and consistency of trace elements and heavy metals using Inductively Coupled Plasma-Mass Spectrometry, and (v) to assess the content of nutritional commercial supplements for steroids, stimulants and other compounds of interest using Tandem Liquid Chromatography-Mass Spectrometry.Methods: The thesis is divided into 6 Chapters. Chapter 1 describes the background to the problem and Chapter 2 reviews the existing legislation. In Chapter 3 the labelling and claims information on 40 nutritional supplements products are analysed, and the self-administered questionnaire determined what product label and other information influences consumers of nutritional supplements in their purchasing decisions. In Chapter 4 the consistency of trace elements and heavy metals are analysed in selected nutritional supplements using Inductively Coupled Plasma Mass Spectrometry. In Chapter 5 selected nutritional supplements are analysed for steroids, stimulants and other compounds using Tandem Liquid Chromatography Mass Spectrometry. All the data of these sections are summarised in Chapter 6. Advisors/Committee Members: Lambert, Mike (advisor), Smith, Peter (advisor).

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Gabriels, G. A. (2013). The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration. (Thesis). University of Cape Town. Retrieved from http://hdl.handle.net/11427/3281

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gabriels, Gary Anthony. “The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration.” 2013. Thesis, University of Cape Town. Accessed March 07, 2021. http://hdl.handle.net/11427/3281.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gabriels, Gary Anthony. “The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration.” 2013. Web. 07 Mar 2021.

Vancouver:

Gabriels GA. The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration. [Internet] [Thesis]. University of Cape Town; 2013. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/11427/3281.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gabriels GA. The investigation and assessment of Nutritional and Traditional Supplement products for content validity, contamination and adulteration. [Thesis]. University of Cape Town; 2013. Available from: http://hdl.handle.net/11427/3281

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Northeastern University

22. Pawar, Grishma. Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease.

Degree: 2019, Northeastern University

URL: http://hdl.handle.net/2047/D20318848

► Chronic neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's diseases (PD) are currently the major health care challenge around the world [1]. The currently… (more)

▼ Chronic neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's diseases (PD) are currently the major health care challenge around the world [1]. The currently used levodopa therapy leads to motor complications like dyskinesias. Invasive techniques like deep brain stimulation used for treating PD leads to nerve cell damage in patients. Delivering drugs in the brain is limited by the presence of the blood brain barrier (BBB). Despite many new developments in the field of CNS drug delivery, overcoming the BBB continues to pose a serious challenge. Parkinson's disease is characterized by the loss of nigrostriatal dopaminergic neurons in turn reducing dopamine levels in brain. Brain-derived neurotropic factor (BDNF) is a high molecular weight protein, responsible for dopaminergic neuron survival [2]. However, the therapeutic applications of BDNF in CNS diseases are limited by the BBB, its complex structure, off-target toxicity, immunogenicity and post-translational modifications. BDNF AntagoNATs (AT's) are small oligonucleotides that can up regulate endogenous BDNF protein expression by inhibiting the natural antisense transcripts (NAT's) and could be a potential therapy for neurodegenerative diseases like AD and PD. The AT's are highly locus specific and are highly stable structures that can improve the uptake of these oligonucleotides in cells. Despite several advantages and significant promise of AT's, they cannot pass through the BBB. In my doctoral project we have successfully developed an innovative endonasal heterotopic mucosal grafting technique that can provide a permanent way of delivering high molecular weight therapeutics like proteins and oligonucleotides to the brain bypassing the BBB. This method is based on human endoscopic skull base surgeries which are currently in practice in the clinic. Using the endonasal mucosal grafting technique, we successfully showed that a model protein like ovalbumin (45 kDa) can be delivered to the brain in spite of its high molecular weight. We utilized a liposome-in gel system to protect the protein from degradation and to allow to sustained drug release. The results of this study were published in PLOS-1 in December 2018 [3]. Regarding BDNF AT's, we have successfully shown the liposomes encapsulating BDNF AT's can up regulate the BDNF mRNA and protein levels in rat schwannoma cells and our results also demonstrate the grafts are capable of delivering therapeutic levels of AT's in rat brain which further resulted in significant protein up regulation in striatum and substantia nigra. We have also shown that the liposomes encapsulating BDNF AT's are capable of protecting dopaminergic neurons in a 6-hydroxydopamine rat model of PD further confirming the therapeutic effect of trans-nasal delivery of BDNF AT's. A manuscript comprising of the results from this study is currently in review in the journal Science Advances. Considering one of the limitations of the mucosal engrafting model being that it allows the delivery of therapeutics from the top of the…

Subjects/Keywords:

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APA (6^th Edition):

Pawar, G. (2019). Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20318848

Chicago Manual of Style (16^th Edition):

Pawar, Grishma. “Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease.” 2019. Doctoral Dissertation, Northeastern University. Accessed March 07, 2021. http://hdl.handle.net/2047/D20318848.

MLA Handbook (7^th Edition):

Pawar, Grishma. “Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease.” 2019. Web. 07 Mar 2021.

Vancouver:

Pawar G. Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease. [Internet] [Doctoral dissertation]. Northeastern University; 2019. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2047/D20318848.

Council of Science Editors:

Pawar G. Trans-nasal Mucosal Delivery Of Bdnf Antagonat Oligonucleotides Using Heterotopic Mucosal Engrafting For Parkinson's Disease. [Doctoral Dissertation]. Northeastern University; 2019. Available from: http://hdl.handle.net/2047/D20318848

University of Iowa

23. Lu, Ko-Ting. Identification of nuclear receptors that regulate renin gene expression.

Degree: MS, Pharmacology, 2014, University of Iowa

URL: https://ir.uiowa.edu/etd/1877

► Renin (REN) expression is required to maintain blood pressure and electrolyte homeostasis. However, the mechanisms by which REN is transcriptionally regulated remain elusive. We… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Lu, K. (2014). Identification of nuclear receptors that regulate renin gene expression. (Masters Thesis). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1877

Chicago Manual of Style (16^th Edition):

Lu, Ko-Ting. “Identification of nuclear receptors that regulate renin gene expression.” 2014. Masters Thesis, University of Iowa. Accessed March 07, 2021. https://ir.uiowa.edu/etd/1877.

MLA Handbook (7^th Edition):

Lu, Ko-Ting. “Identification of nuclear receptors that regulate renin gene expression.” 2014. Web. 07 Mar 2021.

Vancouver:

Lu K. Identification of nuclear receptors that regulate renin gene expression. [Internet] [Masters thesis]. University of Iowa; 2014. [cited 2021 Mar 07]. Available from: https://ir.uiowa.edu/etd/1877.

Council of Science Editors:

Lu K. Identification of nuclear receptors that regulate renin gene expression. [Masters Thesis]. University of Iowa; 2014. Available from: https://ir.uiowa.edu/etd/1877

Columbia University

24. Donthamsetti, Prashant Chandra. Dissecting Dopamine D2 Receptor Signaling.

Degree: 2015, Columbia University

URL: https://doi.org/10.7916/D8QN660V

► Dopamine D2 receptor (D2R) is a G protein-coupled receptor (GPCR) that activates G protein and arrestin signaling molecules. D2R antagonism has been a hallmark of… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Donthamsetti, P. C. (2015). Dissecting Dopamine D2 Receptor Signaling. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8QN660V

Chicago Manual of Style (16^th Edition):

Donthamsetti, Prashant Chandra. “Dissecting Dopamine D2 Receptor Signaling.” 2015. Doctoral Dissertation, Columbia University. Accessed March 07, 2021. https://doi.org/10.7916/D8QN660V.

MLA Handbook (7^th Edition):

Donthamsetti, Prashant Chandra. “Dissecting Dopamine D2 Receptor Signaling.” 2015. Web. 07 Mar 2021.

Vancouver:

Donthamsetti PC. Dissecting Dopamine D2 Receptor Signaling. [Internet] [Doctoral dissertation]. Columbia University; 2015. [cited 2021 Mar 07]. Available from: https://doi.org/10.7916/D8QN660V.

Council of Science Editors:

Donthamsetti PC. Dissecting Dopamine D2 Receptor Signaling. [Doctoral Dissertation]. Columbia University; 2015. Available from: https://doi.org/10.7916/D8QN660V

Boston University

25. Huang, Bryan. Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23720

► BACKGROUND: Obesity has become increasingly prevalent due to over-nutrition and sedentary lifestyle. While many past studies have identified a link between metabolic dysfunction and tissue… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Huang, B. (2017). Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23720

Chicago Manual of Style (16^th Edition):

Huang, Bryan. “Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity.” 2017. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/23720.

MLA Handbook (7^th Edition):

Huang, Bryan. “Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity.” 2017. Web. 07 Mar 2021.

Vancouver:

Huang B. Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/23720.

Council of Science Editors:

Huang B. Toll-like receptor 2 (TLR2) regulates neutrophil production in diet-induced obesity. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23720

Boston University

26. Schlain, Gabrielle Star. Behavioral and pharmacological characterization of a mouse model of palatable diet alternation.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23737

► Obesity and eating disorders represent a severe problem in Western societies. Both the increased availability of highly palatable foods and dieting are major risk factors… (more)

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Schlain, G. S. (2017). Behavioral and pharmacological characterization of a mouse model of palatable diet alternation. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23737

Chicago Manual of Style (16^th Edition):

Schlain, Gabrielle Star. “Behavioral and pharmacological characterization of a mouse model of palatable diet alternation.” 2017. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/23737.

MLA Handbook (7^th Edition):

Schlain, Gabrielle Star. “Behavioral and pharmacological characterization of a mouse model of palatable diet alternation.” 2017. Web. 07 Mar 2021.

Vancouver:

Schlain GS. Behavioral and pharmacological characterization of a mouse model of palatable diet alternation. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/23737.

Council of Science Editors:

Schlain GS. Behavioral and pharmacological characterization of a mouse model of palatable diet alternation. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23737

Boston University

27. Hai, Jerry. Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats.

Degree: MS, Medical Sciences, 2017, Boston University

URL: http://hdl.handle.net/2144/23780

► BACKGROUND: Hypertension is a major health concern with a myriad of possible causes. Sodium is a major component of blood pressure regulation implicated in the… (more)

▼ BACKGROUND: Hypertension is a major health concern with a myriad of possible causes. Sodium is a major component of blood pressure regulation implicated in the maintenance of fluid volume. The blood pressure response to changes in salt intake varies considerably among individuals; salt-sensitive individuals exhibit increases in blood pressure parallel to elevated sodium intake, whereas salt-resistant individuals maintain constant blood pressure regardless of variations in sodium intake. Salt-Sensitive Hypertension (SSH) develops due to an impairment of normal mechanisms that react to an elevated sodium load. Aging is another major risk factor for the development of hypertension. The effects of aging have a profound impact on the cardiovascular, renal, and nervous systems, which work together to regulate blood pressure. The development of SSH and impact of aging on blood pressure have been well-established, but the neurophysiological mechanisms implicated in SSH and aging, have only been recently explored. OBJECTIVE: To provide mechanistic insight regarding the integrated roles of the renal and nervous systems in age-dependent hypertension in male Sprague-Dawley (SD) rats. METHODS: Male SD rats of various ages were randomly assigned to various experimental protocols. 3-month-old male SD rats were randomly assigned to receive Renal-Capsaicin surgery (Renal-CAP) to ablate the afferent renal nerve (ARN) or sham surgery, followed by an acute 5% body weight i.v.-isotonic volume expansion protocol (5%-VE) in which natriuretic response and cardiovascular functions (HR/MAP) were continuously monitored and analyzed for the duration of the experimental period. 3/8/16-month-old male SD rats without Renal-CAP surgery were similarly exposed to the 5%-VE protocol. C-fos immunohistochemistry (c-Fos IHC) was performed on brain slides prepared from rats assigned to the 5%-VE protocol to assess PVN parvocellular neuronal activation, as a marker for ARN activity. 3/8/16-month-old male SD rats on normal-salt and high-salt (NS/HS; 0.6%/4% sodium chloride respectively) diets were assigned to an amiloride and hydrochlorothiazide protocol (AM-HCTZ) to evaluate NCC activity, and exposed to i.p. hexamethonium to account for the sympathetic contribution to blood pressure. Renal/plasma NE content was assessed via ELISA to further account for sympathetic tone. Immunoblotting was performed on 3-month-old control saline-infused, s.c.-norepinephrine (NE), and s.c.-norepinephrine+terazosin/propranolol male SD rats to assess NCC, phosphorylated NCC (pNCCT58), SPAK, WNK1, OxSR1, and phosphorylated OxSR1 protein levels, to evaluate the roles of the α1/β-adrenoceptors in the NCC-implicated ARN-mediated sympathoinhibitory pathway. RESULTS: In response to the 5%-VE protocol, the natriuretic response was attenuated in Renal-Cap rats. Renal-CAP rats also experienced a significant increase in MAP in response to 5%-VE, while sham Renal-CAP rats did not. Both Renal-CAP and sham Renal-CAP rats experienced a significant increase in the mean number of PVN…

Subjects/Keywords: Pharmacology

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APA (6^th Edition):

Hai, J. (2017). Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23780

Chicago Manual of Style (16^th Edition):

Hai, Jerry. “Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats.” 2017. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/23780.

MLA Handbook (7^th Edition):

Hai, Jerry. “Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats.” 2017. Web. 07 Mar 2021.

Vancouver:

Hai J. Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/23780.

Council of Science Editors:

Hai J. Pathophysiology of age-dependent hypertension in male Sprague-Dawley rats. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23780

Boston University

28. Cacace, Hanna. Alternative opioid-sparing treatment options for acute pain management therapy.

Degree: MS, Medical Sciences, 2018, Boston University

URL: http://hdl.handle.net/2144/31158

► The vast array of causes, mechanisms, and interventional strategies for pain has created an extensive field of research spanning a variety of disciplines. This thesis… (more)

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cacace, H. (2018). Alternative opioid-sparing treatment options for acute pain management therapy. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/31158

Chicago Manual of Style (16^th Edition):

Cacace, Hanna. “Alternative opioid-sparing treatment options for acute pain management therapy.” 2018. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/31158.

MLA Handbook (7^th Edition):

Cacace, Hanna. “Alternative opioid-sparing treatment options for acute pain management therapy.” 2018. Web. 07 Mar 2021.

Vancouver:

Cacace H. Alternative opioid-sparing treatment options for acute pain management therapy. [Internet] [Masters thesis]. Boston University; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/31158.

Council of Science Editors:

Cacace H. Alternative opioid-sparing treatment options for acute pain management therapy. [Masters Thesis]. Boston University; 2018. Available from: http://hdl.handle.net/2144/31158

Boston University

29. Mauricio, Ian Paolo Morelos. Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway.

Degree: MS, Medical Sciences, 2018, Boston University

URL: http://hdl.handle.net/2144/31243

► The Hippo tumor suppressor pathway is a highly conserved signaling cascade initially identified in Drosophila which acts to regulate organ size and cellular proliferation. The… (more)

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mauricio, I. P. M. (2018). Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/31243

Chicago Manual of Style (16^th Edition):

Mauricio, Ian Paolo Morelos. “Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway.” 2018. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/31243.

MLA Handbook (7^th Edition):

Mauricio, Ian Paolo Morelos. “Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway.” 2018. Web. 07 Mar 2021.

Vancouver:

Mauricio IPM. Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway. [Internet] [Masters thesis]. Boston University; 2018. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/31243.

Council of Science Editors:

Mauricio IPM. Defining the role of the kinase MST4 in the context of the Hippo tumor suppressor pathway. [Masters Thesis]. Boston University; 2018. Available from: http://hdl.handle.net/2144/31243

Boston University

30. Helfand, Alexander. 3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans.

Degree: MS, Medical Sciences, 2014, Boston University

URL: http://hdl.handle.net/2144/14328

► 3,4-Methylenedioxymethamphetamine (MDMA) is a ring-substituted amphetamine with a potential for abuse. Although originally developed by Merck, MDMA is an illegal drug that is popular recreationally,… (more)

▼ 3,4-Methylenedioxymethamphetamine (MDMA) is a ring-substituted amphetamine with a potential for abuse. Although originally developed by Merck, MDMA is an illegal drug that is popular recreationally, and is more recently being touted as a therapeutic agent. Unlike some other drugs in the amphetamine class, the mechanism(s) by which MDMA produces its subjective effects are not well understood. MDMA is a selective serotonin (5-HT) neurotoxin. Exposure to MDMA can lead to lasting reductions in brain 5-HT and 5-HT axonal markers. Somewhat paradoxically, its acute pharmacological effects involve a dramatic acute increase in serotonin (and other monoamine) levels in the brain and the periphery. MDMA is also a direct agonist at several different monoaminergic receptors. Although these pharmacological properties of MDMA are known, they don't appear to fully explain the subjective of effects of MDMA, which include feelings of well-being and euphoria. One unfortunate notion held by many MDMA users is that the drug is safe, or at least safer than many other illegal drugs. This is a notion that is strengthened by MDMA's current and past use as a psychotherapeutic agent, although definitive safety/efficacy reports have yet to appear in the literature. In recent years, there has been a renewed push to acknowledge the potential utility of MDMA in the treatment of conditions such as post-traumatic stress disorder. MDMA has been reported to damage a number of organ systems in addition to its properties as a selective 5-HT neurotoxin in the brain. Furthermore, recreational MDMA users develop tolerance, which results in a need to increase the dose to achieve the same subjective effects, thereby also increasing the risk for dose-related adverse effects. A number of research laboratories have demonstrated that abstinent MDMA users develop both a loss of brain 5-HT markers, in addition to potential functional consequences of 5-HT neurotoxicity, including deficits in cognitive function, endocrine modulation, and sleep regulation. Although these effects have been well-described, the mechanism by which MDMA leads to neurotoxicity remains unclear, and multiple theories have been suggested. There are many unanswered questions when it comes to MDMA. Without knowing more about how MDMA acts in the body and how it produces toxicities, use of the drug constitutes a significant risk. Not only are the acute, systemic and potentially fatal effects of MDMA problematic, but longer term functional consequences secondary to serotonin depletion may pose significant problems for abstinent MDMA users as they age. In light of the drug's popularity, the need for answers and increased public awareness has never been more pressing. Although MDMA is classified by the Drug Enforcement Agency (DEA) as schedule I, popular musicians have begun to positively reference MDMA in their lyrics, which has likely contributed to the observed rise in MDMA-related hospital visits and fatalities. Communities, parents, and healthcare professionals must make a more…

Subjects/Keywords: Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Helfand, A. (2014). 3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/14328

Chicago Manual of Style (16^th Edition):

Helfand, Alexander. “3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans.” 2014. Masters Thesis, Boston University. Accessed March 07, 2021. http://hdl.handle.net/2144/14328.

MLA Handbook (7^th Edition):

Helfand, Alexander. “3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans.” 2014. Web. 07 Mar 2021.

Vancouver:

Helfand A. 3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans. [Internet] [Masters thesis]. Boston University; 2014. [cited 2021 Mar 07]. Available from: http://hdl.handle.net/2144/14328.

Council of Science Editors:

Helfand A. 3,4-methylenedioxymethamphetamine (MDMA): pharmacology, toxicology, usage patterns, and neurological effects in humans. [Masters Thesis]. Boston University; 2014. Available from: http://hdl.handle.net/2144/14328

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