<p><font size="3"> <p>The blood-brain barrier (BBB) is an interface between the brain parenchyma and the circulating system. This barrier plays a vital role in protecting the CNS by restricting free paracellular diffusion of molecules from the systemic circulation. Methamphetamine (MA) is a highly addictive psychostimulant and has demonstrated neurotoxic properties as well as the ability to compromise the BBB. MA exposure is strongly linked with increased oxidative stress which can result in a decrease in the integrity of the BBB.<font size="3">The aim of this study was to investigate </font><i><font size="3" face="Times New Roman,Times New Roman"><font size="3" face="Times New Roman,Times New Roman">in vitro </font></font><font size="3">effects of pure and street MA &quot / tik&quot / on DNA proliferation and cell cycles in mouse brain endothelial (bEnd5) cells. <font size="3">Trypan blue was used to determine effects of MA (0.0001M-1mM) on cell viability and % cell growth. The Cell Titer Glo&reg / luminescent assay and nonradioactive analogue, 5-bromo-2'-deoxyuridine (BrdU) was used to detect ATP and DNA levels, respectively. Cell cycles (propidium iodide incorporation) were analysed using flow cytometry. Statistical analysis was performed using Wilcoxin Rank Sum Test in which P&lt / 0.05 was denoted as significant. <font size="3">Results of this study showed that:&nbsp / <font size="3">1. Viability of bEnd5 cells exposed to all selected concentrations of MA were unaffected when compared to controls (P&gt / 0.05). <font size="3">2. % Cell growth was suppressed by MA exposure at 96hrs in comparison to that of controls (P&le / 0.03). 3. Cells exposed to MA had significant higher ATP concentrations than control cells at 96hrs (P &le / .0.03) 4. DNA synthesis was markedly suppressed in cells exposed to pure MA and street MA sample 4 (P&le / 0.03), while was similar and higher in cells exposed to street MA sample 1 (P=0.39), and street MA sample 2 and 3 (P&le / 0.04), respectively at 96hrs. 5. bEnd5 cell were arrested between 72 and 96hrs at the G1-S phase. <font size="3">In conclusion, this study demonstrated pure and illicit samples of MA obtained from forensic police did not affect the viability of bEnd5 cells, however resulted in the significant suppression of their cell numbers. This growth inhibition may be due to MA-induced cell cycle arrest at the G1-S phase. The study also showed that compounds found in the samples of street MA produced results significantly different to that of pure MA. </font></font> <p>&nbsp / </p> </font>&nbsp / </font></font></font> <p>&nbsp / </p> </i></p> </font></p> <p>&nbsp / </p>

<p><span style="font-size: 11.5pt">The blood-brain barrier (BBB) is an interface between the brain parenchyma and the circulating system. This barrier plays a vital role in protecting the CNS by restricting free paracellular diffusion of molecules from the systemic circulation. Methamphetamine (MA) is a highly addictive psychostimulant and has demonstrated neurotoxic properties as well as the ability to compromise the BBB. MA exposure is strongly linked with increased oxidative stress which can result in a decrease in the integrity of the BBB. </span></p> <div><span style="font-size: 11.5pt">The aim of this study was to investigate <i>in vitro </i>effects of pure and street MA &ldquo / tik&rdquo / on DNA proliferation and cell cycles in mouse brain endothelial (bEnd5) cells. </span></div> <div><span style="font-size: 11.5pt">Trypan blue was used to determine effects of MA (0.0001M-1mM) on cell viability and % cell growth. The Cell Titer Glo&reg / luminescent assay and nonradioactive analogue, 5-bromo-2'-deoxyuridine (BrdU) was used to detect ATP and DNA levels, respectively. Cell cycles (propidium iodide incorporation) were analysed using flow cytometry. Statistical analysis was performed using Wilcoxin Rank Sum Test in which P&lt / 0.05 was denoted as significant. </span></div> <div><span style="font-size: 11.5pt">Results of this study showed that: </span></div> <div><span style="font-size: 11.5pt">1. Viability of bEnd5 cells exposed to all selected concentrations of MA were unaffected when compared to controls (P&gt / 0.05)&nbsp / </span><span style="font-size: 11.5pt">&nbsp / </span></div> <div><span style="color: windowtext / font-size: 11.5pt">2. % Cell growth was suppressed by MA exposure at 96hrs in comparison to that of controls (P&le / 0.03). </span></div> <div style="margin: 0cm 0cm 25pt"><span style="color: windowtext / font-size: 11.5pt">3. Cells exposed to MA had significant higher ATP concentrations than control cells at 96hrs (P &le / .0.03) </span><span style="color: windowtext / font-size: 11.5pt">4. DNA synthesis was markedly suppressed in cells exposed to pure MA and street MA sample 4 (P&le / 0.03), while was similar and higher in cells exposed to street MA sample 1 (P=0.39), and street MA sample 2 and 3 (P&le / 0.04), respectively at 96hrs. </span><span style="color: windowtext / font-size: 11.5pt">5. bEnd5 cell were arrested between 72 and 96hrs at the G1-S phase.&nbsp / </span></div> <div style="margin: 0cm 0cm 25pt"><span style="line-height: 115% / font-size: 11.5pt">In conclusion, this study demonstrated pure and illicit samples of MA obtained from forensic police did not affect the viability of bEnd5 cells, however resulted in the significant suppression of their cell numbers. This growth inhibition may be due to MA-induced cell cycle arrest at the G1-S phase. The study also showed that compounds found in the samples of street MA produced results significantly different to that of pure MA.</span></div>

<p>This study presents a discursive journey with regard to the risk and protective factors confronting individuals who engage in methamphetamine use within the Manenberg area. Given that this journey requires a cautious and sensitive approach to the meaning making of the lived experiences of the six (6) individual users (the informant base) / the study adopted an analysis process that would allow for a guided &ldquo / tour&rdquo / of these experiences. In doing so, the study made use of the grounded theory method that allowed for this guided &ldquo / tour&rdquo / to be fully anchored in the collected data. External to this data, and once the data emerged as engageable themes, the study introduced, relevantly so, Bronfenbrenner&rsquo / s social-ecological model of human development, so to multiply and deepen the meanings embedded within the data. The merging of this external frame, provided by Bronfenbrenner&rsquo / s model, and the rich data provided by the six (6) informants, uncovered critical themes in understanding the risk and protective factors at play within Manenberg. These themes relate to the historical identity of Manenberg, given the history of Apartheid, the role of the local community and its perceived tolerance of the practice of drug use, which is further echoed in the identity of the family and its limited ability to support drug users in the face of ever-growing poverty. The themes also uncovered the bipolarity in the practice of drug trade and gangsterism as serving a subsistence function, at one level, and an exploitative function at another. Furthermore, the study solidified traditional views that the peer collective is, indeed, a critical actor on the stage of drug use and that the individual (as an actor) continues to be confronted by a script of poverty and disillusionment. This script, as will be illustrated, is also active in preconceived notions of gender stratification.</p>

<p><span style="font-size: 11.5pt">The blood-brain barrier (BBB) is an interface between the brain parenchyma and the circulating system. This barrier plays a vital role in protecting the CNS by restricting free paracellular diffusion of molecules from the systemic circulation. Methamphetamine (MA) is a highly addictive psychostimulant and has demonstrated neurotoxic properties as well as the ability to compromise the BBB. MA exposure is strongly linked with increased oxidative stress which can result in a decrease in the integrity of the BBB. </span></p> <div><span style="font-size: 11.5pt">The aim of this study was to investigate <i>in vitro </i>effects of pure and street MA &ldquo / tik&rdquo / on DNA proliferation and cell cycles in mouse brain endothelial (bEnd5) cells. </span></div> <div><span style="font-size: 11.5pt">Trypan blue was used to determine effects of MA (0.0001M-1mM) on cell viability and % cell growth. The Cell Titer Glo&reg / luminescent assay and nonradioactive analogue, 5-bromo-2'-deoxyuridine (BrdU) was used to detect ATP and DNA levels, respectively. Cell cycles (propidium iodide incorporation) were analysed using flow cytometry. Statistical analysis was performed using Wilcoxin Rank Sum Test in which P&lt / 0.05 was denoted as significant. </span></div> <div><span style="font-size: 11.5pt">Results of this study showed that: </span></div> <div><span style="font-size: 11.5pt">1. Viability of bEnd5 cells exposed to all selected concentrations of MA were unaffected when compared to controls (P&gt / 0.05)&nbsp / </span><span style="font-size: 11.5pt">&nbsp / </span></div> <div><span style="color: windowtext / font-size: 11.5pt">2. % Cell growth was suppressed by MA exposure at 96hrs in comparison to that of controls (P&le / 0.03). </span></div> <div style="margin: 0cm 0cm 25pt"><span style="color: windowtext / font-size: 11.5pt">3. Cells exposed to MA had significant higher ATP concentrations than control cells at 96hrs (P &le / .0.03) </span><span style="color: windowtext / font-size: 11.5pt">4. DNA synthesis was markedly suppressed in cells exposed to pure MA and street MA sample 4 (P&le / 0.03), while was similar and higher in cells exposed to street MA sample 1 (P=0.39), and street MA sample 2 and 3 (P&le / 0.04), respectively at 96hrs. </span><span style="color: windowtext / font-size: 11.5pt">5. bEnd5 cell were arrested between 72 and 96hrs at the G1-S phase.&nbsp / </span></div> <div style="margin: 0cm 0cm 25pt"><span style="line-height: 115% / font-size: 11.5pt">In conclusion, this study demonstrated pure and illicit samples of MA obtained from forensic police did not affect the viability of bEnd5 cells, however resulted in the significant suppression of their cell numbers. This growth inhibition may be due to MA-induced cell cycle arrest at the G1-S phase. The study also showed that compounds found in the samples of street MA produced results significantly different to that of pure MA.</span></div>

Thesis (Ph. D.)--Auburn University. / Abstract. Vita. Includes bibliographical references.

Thesis (M.S.)--University of Tennessee Health Science Center, 2009. / Title from title page screen (viewed on August 5, 2009). Research advisor: David A. Tipton, D.D.S., Ph.D. Document formatted into pages (vi, 39 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 27-38).

Thesis (Ph.D.)--University of Wyoming, 2008. / Title from PDF title page (viewed on August 6, 2009). Includes bibliographical references.

abstract: This dissertation explores the historical development and contemporary deployment of discursive practices that constitute the “truth” of addiction, which in turn serve as the bases for interventions into the lives of people who use intoxicants for any number of reasons. A number of interrelated research questions structure this governmentality analysis. First, what is the evolution of the governmental frames developed and deployed to understand, discipline, and recover addiction in the arena of alcohol and illicit drug use in United States? Second, how does twelve-step serve to transform unruly addicts into self-disciplining citizens? Finally, how does The Meth Project (TMP) exemplify and/or diverge from the dominant addiction governmental frames developed during the Temperance and Progressive eras in the United States? My overall goal is to destabilize our ready understanding of addiction and demonstrate that it is as much a tool of social needs as it is a mental illness by demonstrating: 1) the historically contingent nature of our understandings of addiction and addicts; 2) how these historically contingent understandings are actualized as technologies geared toward “recovering” unruly subjects; and 3) how these historically contingent understandings are taken up as “epistemological scripts” used to conceptualize the “true nature” of certain types of drugs and drug users while simultaneously supporting various regimes of discipline and punishment for those determined to remain “unruly subjects.” / Dissertation/Thesis / Doctoral Dissertation Justice Studies 2016

Magister Psychologiae - MPsych / Substance use addiction is a debilitating and destructive human disorder that affects millions of people worldwide. Of all the provinces in South Africa, the Western Cape has the highest rate of MA use. This highly addictive stimulant, locally known as 'tik', has multiple physiological, psychological, and social effects on the user. The effects are associated with neurocognitive deficits that include deficiencies in working memory and high rates of delay discounting. Current neuropsychopharmacology literature seems to suggest that changes in neurotransmitter functioning and particular brain areas occur that contribute to some of the addictive behaviours associated with chronic MA use. New evidence is emerging that working memory training can help to improve rates of impulsivity in those addicted to MA by strengthening cognitive control. The aim of this project was to establish whether differences in impulse control existed in a sample of 33 male patients at a Western Cape drug rehabilitation centre who received either working memory training with standard drug rehabilitation and or standard drug rehabilitation only. Data was collected with a self-report impulsivity scale (BIS – 11) and analysed using inferential statistics. The results suggest that working memory training, when paired with a standard rehabilitation program, has superior effects in decreasing self-reported rates of impulsivity when compared to standard rehabilitation only. These findings suggest that working memory training may serve as a useful addition to improving impulsivity rates in MA rehabilitation treatment. Further research on a larger scale is required to investigate the findings of this project.

>Magister Scientiae - MSc / The blood-brain barrier (BBB) is an interface between the brain parenchyma and the circulating system. This barrier plays a vital role in protecting the CNS by restricting free paracellular diffusion of molecules from the systemic circulation. Methamphetamine (MA) is a highly addictive psychostimulant and has demonstrated neurotoxic properties as well as the ability to compromise the BBB. MA exposure is strongly linked with increased oxidative stress which can result in a decrease in the integrity of the BBB.The aim of this study was to investigate in vitro effects of pure and street MA "tik" on DNA proliferation and cell cycles in mouse brain endothelial (bEnd5) cells. Trypan blue was used to determine effects of MA (0.0001M-1mM) on cell viability and % cell growth. The Cell Titer Glo® luminescent assay and nonradioactive analogue, 5-bromo-2'-deoxyuridine (BrdU) was used to detect ATP and DNA levels, respectively. Cell cycles (propidium iodide incorporation) were analysed using flow cytometry. Statistical analysis was performed using Wilcoxin Rank Sum Test in which P<0.05 was denoted as significant. Results of this study showed that: 1. Viability of bEnd5 cells exposed to all selected concentrations of MA were unaffected when compared to controls (P>0.05). 2. % Cell growth was suppressed by MA exposure at 96hrs in comparison to that of controls (P≤0.03). 3. Cells exposed to MA had significant higher ATP concentrations than control cells at 96hrs (P ≤.0.03) 4. DNA synthesis was markedly suppressed in cells exposed to pure MA and street MA sample 4 (P≤0.03), while was similar and higher in cells exposed to street MA sample 1 (P=0.39), and street MA sample 2 and 3 (P≤0.04), respectively at 96hrs. 5. bEnd5 cell were arrested between 72 and 96hrs at the G1-S phase. In conclusion, this study demonstrated pure and illicit samples of MA obtained from forensic police did not affect the viability of bEnd5 cells, however resulted in the significant suppression of their cell numbers. This growth inhibition may be due to MA-induced cell cycle arrest at the G1-S phase. The study also showed that compounds found in the samples of street MA produced results significantly different to that of pure MA.