Relevant bibliographies by topics / CNS drugs

Contents

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

Academic literature on the topic 'CNS drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "CNS drugs"

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Generali, Joyce A. "CNS and Psychiatric Drugs." Hospital Pharmacy 37, no. 8 (August 2002): 888–94. http://dx.doi.org/10.1177/001857870203700802.

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“Black-box” warnings report valuable postmarketing safety data about prescription drugs, keeping practitioners informed about potential adverse events, drug interactions, key dosing information, monitoring and administration requirements, and at-risk patient populations. They are especially crucial for newly approved agents. A list of agents with black-box warnings does not currently exist; however Hospital Pharmacy will be publishing comprehensive lists by drug category in this column until November 2002. At that time, a complete list in wall chart form will be released. Hospital Pharmacy will update the data as salient information becomes available.
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Marsden, Charles A., and S. Clare Stanford. "CNS Drugs III: Psychotherapeutics." Expert Opinion on Investigational Drugs 9, no. 8 (August 2000): 1923–29. http://dx.doi.org/10.1517/13543784.9.8.1923.

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Vastag, B. "More Children on CNS Drugs." JAMA: The Journal of the American Medical Association 287, no. 15 (April 17, 2002): 1930—a—1930. http://dx.doi.org/10.1001/jama.287.15.1930-a.

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Vastag, Brian. "More Children on CNS Drugs." JAMA 287, no. 15 (April 17, 2002): 1930. http://dx.doi.org/10.1001/jama.287.15.1930-jha20004-2-1.

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Schou, Magnus, and Katarina Varnäs. "PET microdosing of CNS drugs." Clinical and Translational Imaging 5, no. 3 (March 23, 2017): 291–98. http://dx.doi.org/10.1007/s40336-017-0226-y.

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Tobinick, Edward Lewis. "Perispinal Delivery of CNS Drugs." CNS Drugs 30, no. 6 (April 27, 2016): 469–80. http://dx.doi.org/10.1007/s40263-016-0339-2.

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&NA;. "Elderly less tolerant of CNS drugs." Reactions Weekly &NA;, no. 501 (May 1994): 3. http://dx.doi.org/10.2165/00128415-199405010-00005.

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Ghose, Karabi. "Prescribing CNS Drugs for Elderly Patients." Drugs & Aging 4, no. 4 (April 1994): 275–84. http://dx.doi.org/10.2165/00002512-199404040-00001.

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BOSCHERT, SHERRY. "CNS Drugs And Cognitive Decline Tied." Family Practice News 38, no. 4 (February 2008): 34. http://dx.doi.org/10.1016/s0300-7073(08)70241-x.

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Preskorn, Sheldon H. "CNS Drug Development: Part I: The Early Period of CNS Drugs." Journal of Psychiatric Practice 16, no. 5 (September 2010): 334–39. http://dx.doi.org/10.1097/01.pra.0000388628.44405.c0.

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Dissertations / Theses on the topic "CNS drugs"

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Kyles, Andrew Edward. "Evaluation of the spinal and supraspinal roles of antinociceptive drugs in sheep." Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389998.

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Rahman, Shazia. "Use of (2S)-pyroglutamic acid for the synthesis of glutamate agonists and antagonists and 1-#beta#-methylcarbapenams." Thesis, University of Sussex, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264581.

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Sekhar, Gayathri Nair. "The transport of CNS-active cationic drugs across the blood-brain barrier." Thesis, King's College London (University of London), 2016. https://kclpure.kcl.ac.uk/portal/en/theses/the-transport-of-cnsactive-cationic-drugs-across-the-bloodbrain-barrier(41ff27df-17ce-4edc-82fe-c4169edf801c).html.

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The physical, transport, and metabolic barriers presented by the cerebral microvessel endothelium - the blood- brain barrier (BBB) - protect the brain from damage from toxic substances and ensure the delivery of nutrients required for the functioning of the brain thus creating a stable neuronal microenvironment. However, the BBB poses a challenge to many CNS-active drugs which must cross the BBB to reach their target. Of the drugs that target the brain, many are cationic at physiological pH making their transport into the brain even harder with the additional potential for drug-drug interactions. Therefore, this thesis has been an attempt to understand the transport characteristics of cationic therapeutic drugs across the BBB. One of the foci of this study has been the anti-human African trypanosomiasis (HAT) drugs pentamidine and e ornithine, both positively charged at physiological pH. Pentamidine is a stage 1 drug for HAT that was previously found in our laboratory to not cross the mouse BBB in vivo as it was a substrate for eux transporters, particularly P-glycoprotein. The present study observed that pentamidine is taken up by Organic Cation Transporter 1 (OCT1) in hCMEC/D3 (human) and bEnd.3 (mouse) cell lines where it accumulates and is euxed by ATP-dependent mechanisms out of the cell. In addition, the predominant localisation of OCT1 at the luminal membrane of the BBB may explain the low permeability of pentamidine into the brain. Considering pentamidine is a substrate for P-glycoprotein at the BBB, inhibitors of Pglycoprotein were used to increase pentamidine delivery into the brain. Pluronic® triblock polymers P85, P105, and F68 were thus chosen for their proven ability to inhibit P-glycoprotein and for their promising results from clinical trials. They were used at concentrations of 0.01%, 0.025%, 0.1%, and 0.5% along with pentamidine in an attempt to increase its delivery across the BBB, concomitantly reducing any side-e ects. In vitro assays carried out on MDCK-hMDR cell line suggested high concentrations of P85 and P105 were cytotoxic even though P85 was able to signi cantly increase pentamidine permeability at 0.5% and 0.1%. Greater speci city to a target could circumvent toxicity issues in the future. The second anti-HAT drug studied was e ornithine that treats stage 2 of HAT. To treat stage 2 of the disease it must cross the BBB, yet it was not found to cross the BBB in the in vivo study on mice carried out in our laboratory. Results obtained from assessing the accumulation of e ornithine in hCMEC/D3 and bEnd.3 cell lines, the in vitro models of the BBB, also suggested limited entry of e ornithine into the BBB. Nonetheless, the assays indicated that e ornithine could be a weak substrate for system y+ at the BBB. There was also evidence for its interaction with OCTs in the bEnd.3 cell line. Second part of the thesis focussed on the antipsychotic drugs haloperidol and amisulpride, both cationic drugs at physiological pH. Haloperidol, an extensively used drug both as an antipsychotic and for palliative care, has the potential to interact with other drugs at the BBB. Haloperidol was found to be a substrate for OCTs at the BBB in both hCMEC/D3 and bEnd.3 cell lines and was found to accumulate readily inside the BBB cells. Similarly, amisulpride is an antipsychotic that is also used to treat delusions and aggression in Alzheimer's disease (AD). Previous studies found increased central dopamine receptor occupancy in AD patients when amisulpride was administered at very low doses. Unlike haloperidol, amisulpride had very low accumulation inside the BBB cells. Results suggested amisulpride to be a substrate for the OCTs and the eux transporters MATE1 and PMAT at the BBB. Amisulpride entry into the brain was also tested in wildtype and transgenic AD mice to nd that amisulpride entry into the transgenic mice brains was signi cantly greater than wildtype mice brains and this was not due to a `leaky' BBB of the AD model. Changes to the expression levels of OCT1, 2, 3 and P-glycoprotein transporters in wildtype and AD model mice BBB were determined using Western blotting and no di erences were found. Further exploration of capillaries isolated from human brain samples from control and AD a ected patients was carried out and signi cant region-speci c changes to the expression levels of MATE1 was observed. There was also a tendency for region-speci c decrease in PMAT expression levels. MATE1 and PMAT are proton-dependent transporters that eux substrates out of the BBB. This decrease in eux transporter expression at the BBB of AD patients could explain the increased sensitivity in AD patients to amisulpride.
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Lloyd, Edward John, and mikewood@deakin edu au. "A common structural basis for central nervous system drug design." Deakin University. School of Biological Sciences, 1986. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050902.115505.

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The main theme of this thesis is that there is a common structural basis for drugs acting on the central nervous system (CNS), and that this concept may be used to design new CNS-active drugs which have greater specificity and hence less side-effects. To develop these ideas, the biological basis of how drugs modify CMS neurotransmission is described, and illustrated using dopaminergic pathways. An account is then given of the use of physicochemical concepts in contemporary drug design. The complete conformational analysis of several antipsychotic drugs is used to illustrate some of these techniques in the development of a model for antipsychotic drug action. After reviewing current structure-activity studies in several classes of CNS drugs (antipsychotics, anti-depressants, stimulants, hal1ucinogens, anticonvulsants and analgesics), a hypothesis for a common structural basis of CNS drug action is proposed- This is based on a topographical comparison of the X-ray structures of eight representative CNS-active drugs, and consists of three parts: 1.there is a common structural basis for the activity of many different CNS-active drug classes; 2. an aromatic ring and a nitrogen atom are the primary binding groups whose topographical arrangement is fundamental to the activity of these drug classes; 3. the nature and placement of secondary binding determines different classes of CNS drug activity. A four-Point model for this common structural basis is then defined using 14- CNS-active drug structures that include the original eight used in proposing the hypothesis. The coordinates of this model are: R1 (0. 3.5, 0), R2 (0, -3.5, O), N (4.8. -0.3, 1.4), and R3 (6.3, 1.3, 0), where R1 and R2 represent the point locations of a hydrophobic interaction of the common aromatic ring with a receptor, and R3 locates the receptor point for a hydrogen bond involving the common nitrogen, N. Extended structures were used to define the receptor points R1, R2 and R3, and the complete conformational space of each of the 14 molecules was considered. It is then shoun that the model may be used to predict whether a given structure is likely to show CNS activity: a search over 1,000 entries in the current Merck Index shows a high probability (82%) of CNS activity in compounds fitting the structural model. Analysis of CNS neurotransmitters and neuropeptides shows that these fit the common model well. Based on the available evidence supporting chemical evolution, protein evolution, and the evolution of neurotransmitter functions, it is surmised that the aromatic ring/nitrogen atom pharmacophore proposed in the common model supports the idea of the evolution of CNS receptors and their neurotransmitters, possibly from an aromatic amine or acety1cho1ine acting as a primaeval communicating molecule. The third point in the hypothesis trilogy is then addressed. The extensive conformation-activity analyses that have resulted in well-defined models for five separate CNS drug classes are used to map out the locations of secondary binding groups relative to the common model for anti-psychotics, antidepressants, analgesics, anticholinergics, and anticonvulsants. With this information, and knowledge derived from receptor-binding data, it is postulated that drugs having specified activity could be designed. In order to generate novel structures having a high probability of CNS-activity, a process of drug design is described in which known CNS structures are superimposed topographically using the common model as a template. Atoms regarded as superfluous may be selectively deleted and the required secondary binding groups added in predicted locations to give novel structures. It is concluded that this process provides the basis for the rational design of new lead compounds which could further be optimized for potent and specific CNS activity.
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Berggård, Cecilia. "Transcription Factor AP-2 in Relation to Personality and Antidepressant Drugs." Doctoral thesis, Uppsala University, Department of Neuroscience, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4638.

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The CNS monoaminergic systems are considered as the head engine regulating neuropsychiatric functions and personality. Transcription factor AP-2 is known to be essential for the development of the brainstem including the monoaminergic nuclei, and has the ability to regulate many genes in the monoaminergic systems. The ability of transcription factors to regulate specific gene expression, has lately made them hot candidates as drug targets. In this thesis, results indicating a role of AP-2 in the molecular effects of the antidepressant drugs citalopram and phenelzine, are presented.

A polymorphism in the second intron of the gene encoding AP-2ß has previously been associated with anxiety-related personality traits as estimated by the Karolinska Scales of Personality (KSP). In this thesis, results confirming this association, gained by using a larger material and several different personality scales, are presented. Furthermore, data is presented showing an association between the activity of platelet monoamine oxidase, a trait-dependent marker for personality, and the genotype of the AP-2ß intron 2 polymorphism.

The functional importance of the AP-2ß intron 2 polymorphism has not yet been elucidated. Included in this thesis are results showing that the AP-2ß intron 2 polymorphism is not in linkage disequilibrium with the only other described polymorphism in the AP-2ß gene, i.e. in the AP-2ß promoter (-67 G/A). Introns have in several studies been shown to include binding sites for regulatory proteins, and thus, to be important in transcriptional regulation. Results are presented demonstrating that one human brain nuclear protein binds only to the long variant of the AP-2ß intron 2 polymorphism. If this protein is involved in the regulation of the AP-2ß gene, it would affect the expression levels of the AP-2ß protein.

In general, this thesis further establishes the role of transcription factor AP-2 as a regulatory factor of importance for personality and monoaminergic functions.

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Patel, Sulay H. "Effects of HIV-1 Tat and drugs of abuse on antiretroviral penetration inside different CNS cell types." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5685.

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Human immunodeficiency (HIV) infection can result in neurocognitive deficits in about one-half of infected individuals. Despite excellent systemic effectiveness, restricted antiretroviral penetration across the blood-brain barrier (BBB) is a major limitation in fighting HIV infection within the central nervous system (CNS). Drug abuse exacerbates cognitive impairment and pathologic CNS changes in HIV-infected individuals. This work investigates the effects of the HIV-1 protein, Tat, and drugs of abuse on factors affecting drug penetration into the brain. Firstly, an in vitro model of the blood-brain barrier was built to study effects of HIV-1 Tat and methamphetamine (Meth) on integrity and function of the BBB, in turn how HIV-1 Tat and meth will affect antiretroviral penetration into the brain. We found that co-exposure HIV-1 Tat and Meth results in inhibition or impairment of P-glycoprotein activity at the BBB. Also, simultaneous inhibition of P-glycoprotein (P-gp) and Multidrug Resistant Protein -1 (MRP-1), by verapamil and MK-571 causes an increase in accumulation of atazanavir inside the primary human brain endothelial cells. Secondly, we developed and validated the method for simultaneous determination of tenofovir, emtricitabine, and dolutegravir in cell extracts of CNS cells. This method was used to study how HIV-1 Tat and/or morphine affects antiretroviral penetration in CNS cells like human brain microvascular endothelial cells, human astrocytes, human microglia, and human pericytes. We found that in untreated cells, accumulation of antiretroviral drugs was higher in hCMEC/D3 cells compared to other CNS cell types. Also, HIV-1 Tat and/or morphine had no significant effect on antiretroviral penetration amongst these cell types. Overall, the rank order of intracellular accumulation observed in treated and untreated cells was dolutegravir > emtricitabine > tenofovir.
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Garcia-Mijares, Miriam. "Efeito da administração aguda e repetida de fencanfamina sobre o valor reforçado do estímulo." Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-14092006-114120/.

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A fencanfamina (FCF) é um agonista indireto do sistema dopaminérgico que tem efeitos neurais e comportamentais similares aos observados com outras drogas estimulantes como a anfetamina ou a cocaína (COC). O presente trabalho teve como objetivo avaliar o efeito da administração aguda e repetida de FCF sobre o valor reforçador dos estímulos (Re). Foi usada a equação de igualação proposta por Herrnstein (1970) para avaliar esse efeito motivacional Foi também medido o efeito dessa droga sobre a taxa de respostas e a capacidade motora (k). Três experimentos foram realizados. Nos três experimentos o efeito da FCF foi testado em ratos treinados em um esquema múltiplo de sete componentes de diferentes Vls. Nos Experimentos 1 e 2 (E1 e E2, respectivamente) três doses agudas de FCF (0,88 mg/kg, 1,75 mg/kg e 3,5 mg/kg) foram administradas i.p. No E1 o reforçador foi água e no E2 reforçador foi sacarose. Em ambos os experimentos, o efeito da droga sobre os parâmetros estudados foi semelhante: as três doses de FCF aumentaram a taxa de respostas e diminuíram Re, sem alterar k. No Experimento 3, seis injeções de veiculo (Grupo VEI) ou de 1,75 mg/kg de FCF (Grupo DROGA) foram administradas i.p. intermitentemente aos sujeitos a fim de promover sensibilização comportamental. Após sete dias de suspensão da droga, foi administrada uma dose de 0,88 mg/kg de FCF em animais de ambos os grupos e foi medido o efeito sobre a taxa de respostas, k e Re. Os resultados obtidos mostraram que a administração repetida de FCF não alterou o efeito dessa droga sobre os parâmetros estudados. Os resultados são consistentes com os dados que mostram que a FCF tem efeitos sobre o comportamento similares aos de outros estimulantes, e apoiam a hipótese de que o aumento da taxa de respostas observado após a administração da FCF está relacionado a mudanças no valor reforçador dos estímulos, o que sugere um efeito motivacional e não motor. Além disso, os resultados sustentam as hipóteses que relacionam o sistema dopaminérgico ao processo do reforço. A falha na obtenção de sensibilização após a administração repetida de FCF poderia estar relacionada à dose utilizada ou ao numero de injeções administradas.
Fencanfamina (FCF) is an indirect dopaminergic agonist with neural and behavioral effects similar to those observed for other stimulant drugs such as the amphetamine or cocaine (COC). The aim of the present investigation was to evaluate the effect of acute and repeated administration of FCF on the reinforcing value (Re) taken as a motivational index. The Herrnstein hyperbole equation (1970) was used to evaluate this motivacional effect. The effects of FCF on response rate and motor capacity (k) where also observed. Three experiments were conducted. In all of them the effect of FCF was tested on rats trained on seven VI multiple schedule. In Experiments 1 and 2 (E1 and E2, respectively) three acute doses of FCF (0.88 mg/kg, 1.75 mg/kg and 3.5 mg/kg) were administered (i.p.) The reinforcer was water (E1) or sacarose (E2). In both experiments, the effect of the drug on the parameters studied was similar: the three doses of FCF increased the response rate, decreased Re and had no effect on k. In Experiment 3, six injections of vehicle (VEI Group) or 1.75 mg/kg of FCF (DROGA Group) were intermittently administered (i.p.) in order to promote sensitization. Seven days after drug withdrawal a single dose of 0.88 mg/kg of FCF was administered to animals in both groups and the effect on response rate, k and Re was measured. Results showed that repeated administration of FCF did not change the effect of this drug on the parameters investigated. These results are consistent with the evidence showing that FCF has behavioral effects similar to those reported for other stimulants and support the interpretation that increases in response rate are primarily related to changes in reinforcing value. Thus they probably reflect a motivational effect of the drug. Moreover, the results support the hypotheses that associate the dopaminergic system to the process of reinforcement. It is speculate that the failure to obtain sensitization after repeated administration of FCF could be related to dosage or number of injections.
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Mercolini, Laura <1979&gt. "Development of original analytical methods for the therapeutic drug monitoring of CNS druges: Antipsychotics, Antidepressants and Anxiolytics-hypnotics." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2713/.

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Great strides have been made in the last few years in the pharmacological treatment of neuropsychiatric disorders, with the introduction into the therapy of several new and more efficient agents, which have improved the quality of life of many patients. Despite these advances, a large percentage of patients is still considered “non-responder” to the therapy, not drawing any benefits from it. Moreover, these patients have a peculiar therapeutic profile, due to the very frequent application of polypharmacy, attempting to obtain satisfactory remission of the multiple aspects of psychiatric syndromes. Therapy is heavily individualised and switching from one therapeutic agent to another is quite frequent. One of the main problems of this situation is the possibility of unwanted or unexpected pharmacological interactions, which can occur both during polypharmacy and during switching. Simultaneous administration of psychiatric drugs can easily lead to interactions if one of the administered compounds influences the metabolism of the others. Impaired CYP450 function due to inhibition of the enzyme is frequent. Other metabolic pathways, such as glucuronidation, can also be influenced. The Therapeutic Drug Monitoring (TDM) of psychotropic drugs is an important tool for treatment personalisation and optimisation. It deals with the determination of parent drugs and metabolites plasma levels, in order to monitor them over time and to compare these findings with clinical data. This allows establishing chemical-clinical correlations (such as those between administered dose and therapeutic and side effects), which are essential to obtain the maximum therapeutic efficacy, while minimising side and toxic effects. It is evident the importance of developing sensitive and selective analytical methods for the determination of the administered drugs and their main metabolites, in order to obtain reliable data that can correctly support clinical decisions. During the three years of Ph.D. program, some analytical methods based on HPLC have been developed, validated and successfully applied to the TDM of psychiatric patients undergoing treatment with drugs belonging to following classes: antipsychotics, antidepressants and anxiolytic-hypnotics. The biological matrices which have been processed were: blood, plasma, serum, saliva, urine, hair and rat brain. Among antipsychotics, both atypical and classical agents have been considered, such as haloperidol, chlorpromazine, clotiapine, loxapine, risperidone (and 9-hydroxyrisperidone), clozapine (as well as N-desmethylclozapine and clozapine N-oxide) and quetiapine. While the need for an accurate TDM of schizophrenic patients is being increasingly recognized by psychiatrists, only in the last few years the same attention is being paid to the TDM of depressed patients. This is leading to the acknowledgment that depression pharmacotherapy can greatly benefit from the accurate application of TDM. For this reason, the research activity has also been focused on first and second-generation antidepressant agents, like triciclic antidepressants, trazodone and m-chlorophenylpiperazine (m-cpp), paroxetine and its three main metabolites, venlafaxine and its active metabolite, and the most recent antidepressant introduced into the market, duloxetine. Among anxiolytics-hypnotics, benzodiazepines are very often involved in the pharmacotherapy of depression for the relief of anxious components; for this reason, it is useful to monitor these drugs, especially in cases of polypharmacy. The results obtained during these three years of Ph.D. program are reliable and the developed HPLC methods are suitable for the qualitative and quantitative determination of CNS drugs in biological fluids for TDM purposes.
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Jain, Anjana. "Delivery of Cdc42, Rac1, and Brain-derived Neurotrophic Factor to Promote Axonal Outgrowth After Spinal Cord Injury." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/16210.

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Injury severs the axons in the spinal cord causing permanent functional loss. After injury, a series of events occur around the lesion site, including the deposition of growth cone inhibitory astroglial scar tissue containing chondroitin sulfate proteoglycan (CSPG)- rich regions. It is important to encourage axons to extend through these inhibitory regions for regeneration to occur. The work presented in this dissertation investigates the effect of three proteins, constitutively active (CA)-Cdc42, CA-Rac1, and brain-derived neurotrophic factor (BDNF) on axonal outgrowth through CSPGs-rich inhibitory regions after spinal cord injury (SCI). Cdc42 and Rac1 are members of the Rho GTPase family and BDNF is a member of the neurotrophin sub-family. These three proteins affect the actin cytoskeleton dynamics. Therefore, Cdc42, Rac1, and BDNF promote axonal outgrowth. The effect of CA-Cdc42 and CA-Rac1 on neurite extension through CSPG regions was determined in an in vitro model. Rac1 and Cdc42 s ability to modulate CSPG-dependent inhibition has yet to be explored. In this study, a stripe assay was utilized to examine the effects of modulating all three Rho GTPases on neurite extension across inhibitory CSPG lanes. Alternating laminin (LN) and CSPG lanes were created and NG108-15 cells and E9 chick dorsal root ganglions (DRGs), were cultured on the lanes. Using the protein delivery agent Chariot, the neuronal response to exposure of CA and dominant negative (DN) Rho GTPases, along with the bacterial toxin C3, was determined by quantifying the percent ratio of neurites crossing the CSPG lanes. CA-Cdc42, CA-Rac1, and C3 transferase significantly increased the number of neurites crossing into the CSPG lanes compared to the negative controls for both the NG108-15 cells and the E9 chick DRGs. We also show that these mutant proteins require the delivery vehicle, Chariot, to enter the neurons and affect neurite extension. Therefore, activation of Cdc42 and Rac helps overcome the CSPG-dependent inhibition of neurite extension. In an in vivo study, CA-Cdc42 and CA-Rac1 were locally delivered into a spinal cord cavity. Additionally, BDNF was delivered to the lesion site, either individually or in combination with either CA-Cdc42 or CA-Rac1. The dorsal over-hemisection model was utilized, creating a ~2mm defect that was filled with an in situ gelling hydrogel scaffold containing lipid microtubules loaded with the protein(s) to encourage axons. The lipid microtubules enable slow release of proteins while the hydrogel serves to localize them to the lesion site and permit axonal growth. The results from this study demonstrate that groups treated with BDNF, CA-Cdc42, CA-Rac1, BDNF/CA-Cdc42, and BDNF/CA-Rac1 had significantly higher percentage of axons from the corticospinal tract (CST) that traversed the CSPG-inhibitory regions, as well as penetrate the glial scar compared to the untreated and agarose controls. Although axons from the CST tract did not infiltrate the scaffold-filled lesion, NF-160+ axons were observed in the scaffold. Treatment with BDNF, CA-Cdc42, and CA-Rac1 also reduced the inflammatory response, quantified by analyzing GFAP and CS-56 intensity for reactive astrocytes and CSPGs, respectively, at the interface of the scaffold and host tissue. Therefore, the local delivery of CA-Cdc42, CA-Rac1 and BDNF, individual and combination demonstrated the ability of axons to extend through CSPG inhibitory regions, as well as reduce the glial scar components.
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Fidanboylu, Mehmet. "Blood-CNS transport mechanisms in pathophysiology and drug delivery." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/bloodcns-transport-mechanisms-in-pathophysiology-and-drug-delivery(2081d984-07fe-41aa-9f5b-54d1f33be9f2).html.

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The blood-CNS barriers form a highly selective biological firewall; regulating the passage of solutes between the blood and cerebral microenvironment. This thesis modelled the blood-CNS barriers in vivo to determine the transport of nutrients, metabolic products and drugs across these barriers, and was split into two main parts: 1. L-arginine and ADMA transport - Circulating levels of the cationic amino acid L-arginine and its endogenously produced homologue asymmetric dimethylarginine (ADMA) are in delicately poised equilibrium. Dysregulation of this balance has well-documented implications in cardiovascular disease and also more recently conditions of the brain, as ADMA is a potent inhibitor of nitric oxide synthase (NOS) enzymes, including the endothelial (eNOS) and neuronal (nNOS) isoforms. Until now it has been postulated that ADMA competes for transport across membranes via the same cationic transport system as L-arginine (system y+), however this hypothesis has surprisingly never been tested. The major contributors to transport of both amino acids were investigated to determine how their respective intracellular and extracellular concentrations affect transport across the blood-CNS barriers. These data also have strong relevance to other research areas due to the widespread influence of NO in physiological pathways in health and disease. At the time of writing, this study represents the first true characterisation of ADMA transport across any physiological membrane in vivo and reveals a likely mechanism for explaining ‘the L-arginine paradox’ – the clinical observation that NO-deficient patients respond well to oral supplementation with L-arginine even though [arginine]plasma is easily sufficient to saturate eNOS. 2. ‘NanoHAT’ - Efflux transporters expressed at the blood-CNS barriers remain one of the biggest hurdles for the efficient delivery of therapeutic agents to the brain. The anti-trypanosomal drug pentamidine was shown previously by our group to be a substrate for efflux from the blood-CNS barriers and does not ordinarily accumulate to pharmacologically relevant levels in the brain. Pluronic® copolymers are known biological response modifiers that are approved for use in humans and have generated a great deal of interest due to their ability to inhibit efflux transporters and spontaneously form micelles in solution. In this study, a coformulation of pentamidine and Pluronic® P85 was evaluated as a potential future treatment for CNS-stage Human African Trypanosomiasis, using a combination of in silico, in vitro, and in vivo methodologies. Combining our group’s knowledge and expertise in blood-brain barrier research with colleagues in Molecular Biophysics and Materials & Molecular Modelling has resulted in the creation of a ‘mini formulation-development pathway’ that can be utilised to optimise and develop formulations in the future.
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Books on the topic "CNS drugs"

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International Bioanalytical Forum (6th 1985 University of Surrey). Bioactive analytes: Including CNS drugs, peptides, and enantiomers. New York: Plenum Press, 1986.

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Reid, Eric, Bryan Scales, and Ian D. Wilson, eds. BIOACTIVE ANALYTES, Including CNS Drugs, Peptides, and Enantiomers. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1892-8.

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McArthur, Robert A., and Franco Borsini. Animal and translational models for CNS drug discovery. Amsterdam: Elsevier/Academic Press, 2008.

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Kalali, Amir, Joseph Kwentus, Sheldon Preskorn, and Stephen M. Stahl, eds. Essential CNS Drug Development. Cambridge: Cambridge University Press, 2012. http://dx.doi.org/10.1017/cbo9780511977640.

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Essential CNS drug development. Cambridge: Cambridge University Press, 2012.

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Schreiber, Rudy, ed. Modern CNS Drug Discovery. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62351-7.

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Borsook, David, Lino R. Beccera, Edward Bullmore, and Richard J. Hargreaves, eds. Imaging in CNS Drug Discovery and Development. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0134-7.

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Atta-ur-Rahman and M. Iqbal Choudhary, eds. Frontiers in CNS Drug Discovery Volume 3. UAE: Bentham Science Publishers Ltd., 2017. http://dx.doi.org/10.2174/97816810844351170301.

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Ces drôles de médicaments. Paris: Delagrange, 1990.

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Concise clinical pharmacology: CNS therapeutics. New York: McGraw-Hill, Medical Pub. Division, 2007.

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Book chapters on the topic "CNS drugs"

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Lowe, John A. "CNS Drugs." In Drug Discovery, 245–86. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118354483.ch7.

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Buccafusco, Jerry J., and Moussa B. H. Youdim. "Drugs with multiple CNS targets." In Cognitive Enhancing Drugs, 179–98. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7867-8_11.

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Bhandari, Prasan. "CNS stimulants/drugs of abuse." In Pharmacology Mind Maps for Medical Students and Allied Health Professionals, 274–80. Boca Raton, FL : CRC Press/Taylor & Francis, 2020.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429023859-30.

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Riedel, Wim. "The Special Challenges of Developing CNS Drugs." In Modern CNS Drug Discovery, 231–34. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62351-7_15.

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Wenger, Galen R. "CNS Stimulants and Athletic Performance." In Drugs, Athletes, and Physical Performance, 217–34. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5499-4_14.

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Rankovic, Zoran. "Designing CNS Drugs for Optimal Brain Exposure." In Blood-Brain Barrier in Drug Discovery, 385–424. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118788523.ch18.

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Nemes, András. "Monoterpenoid Indole Alkaloids, CNS and Anticancer Drugs." In Analogue-Based Drug Discovery II, 189–215. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527630035.ch8.

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Caddy, B., and W. M. L. Chow. "Novel Capillary Gas-Chromatographic Phases Applicable to Drugs." In BIOACTIVE ANALYTES, Including CNS Drugs, Peptides, and Enantiomers, 221–34. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1892-8_18.

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Feitsma, Karla G., Ben F. H. Drenth, Kor H. Kooi, Jan Bosman, and Rokus A. de Zeeuw. "Attempts to Obtain Separations of Chiral Anticholinergic Drugs." In BIOACTIVE ANALYTES, Including CNS Drugs, Peptides, and Enantiomers, 259–69. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4757-1892-8_21.

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Verster, Joris C. "Effects of CNS-Drugs and Alcohol on Driving Ability." In Sleepiness and Human Impact Assessment, 113–19. Milano: Springer Milan, 2014. http://dx.doi.org/10.1007/978-88-470-5388-5_10.

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Conference papers on the topic "CNS drugs"

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Batchu, Jayanth V. N., and Abasifreke U. Ebong. "Photovoltaic therapy: Conceptual nanoscopic photovoltaic device for transporting chemotherapeutic drugs." In 2013 10th International Conference on High Capacity Optical Networks and Enabling Technologies (HONET-CNS). IEEE, 2013. http://dx.doi.org/10.1109/honet.2013.6729760.

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Kim, Jung Hwan, Garrett W. Astary, Thomas H. Mareci, and Malisa Sarntinoranont. "A Computational Model of Direct Infusion Into the Rat Brain: Corpus Callosum and Hippocampus." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205945.

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Despite the high therapeutic potential of many macromolecular drugs, it has proven difficult to apply them to treatment of cancer and other degenerative diseases of the central nervous system (CNS) due to low capillary permeability and low diffusivity. To overcome these barriers, recent experimental studies have shown local infusion, i.e., convection-enhanced delivery (CED), to be a promising delivery technique in the brain and spinal cord [1–3]. Predictive models of extracellular fluid flow and transport during CED would be useful for treatment optimization and planning.
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Lueshen, Eric, Indu Venugopal, and Andreas Linninger. "Intrathecal Magnetic Drug Targeting: A New Approach to Treating Diseases of the Central Nervous System." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93117.

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Intrathecal (IT) drug delivery is a standard technique which involves direct injection of drugs into the cerebrospinal fluid (CSF)-filled space within the spinal canal to treat many diseases of the central nervous system. Currently, in order to reach the therapeutic drug concentration at certain locations within the spinal canal, high drug doses are used. With no method to deliver the large drug doses locally, current IT drug delivery treatments are hindered with wide drug distributions throughout the central nervous system (CNS) which cause harmful side effects. In order to overcome the current limitations of IT drug delivery, we have developed the novel method of intrathecal magnetic drug targeting (IT-MDT). Gold-coated magnetite nanoparticles are infused into a physiologically and anatomically relevant in vitro human spine model and then targeted to a specific site using external magnetic fields, resulting in a substantial increase in therapeutic nanoparticle localization at the site of interest. Experiments aiming to determine the effect of key parameters such as magnet strength, duration of magnetic field exposure, location of magnetic field, and ferrous implants on the collection efficiency of our superparamagnetic nanoparticles in the targeting region were performed. Our experiments indicate that intrathecal magnetic drug targeting and implant-assisted IT-MDT are promising techniques for concentrating and localizing drug-functionalized nanoparticles at required target sites within the spinal canal for potential treatment of diseases affecting the central nervous system.
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Labrecque, S., J. P. Sylvestre, S. Marcet, F. Mangiarini, M. Verhaegen, P. De Koninck, and S. Blais-Ouellette. "Hyperspectral imaging to monitor simultaneously multiple protein subtypes and live track their spatial dynamics: a new platform to screen drugs for CNS diseases." In SPIE BiOS, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2015. http://dx.doi.org/10.1117/12.2079882.

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Bhosle, Abhinav, Pratibha Singhal, Vibhor Pardasani, Prajay Lunia, Kanchan Ajbani, Dipak Dhangar, and Suhas Tiple. "Pyrosequencing(PSQ) in early diagnosis of CNS tuberculosis and determining drug resistance." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4590.

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Iliescu, Ciprian, Bangtao Chen, Jiashen Wei, and Zhilian Yue. "Transdermal drug delivery: Microfabrication insights." In 2009 International Semiconductor Conference (CAS 2009). IEEE, 2009. http://dx.doi.org/10.1109/smicnd.2009.5336568.

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Salvador, Ellaine, Almuth F. Kessler, Julia Hörmann, Malgorzata Burek, Catherine T. Brami, Tali V. Sela, Moshe Giladi, et al. "Abstract 6251: Blood brain barrier opening by TTFields: a future CNS drug delivery strategy." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6251.

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Doutremepuich, C., O. de Sèze, T. Castrioto, F. Peirera, F. Doutremepuich, and F. Toulemonde. "TREATMENT OF EXPERIMENTAL VENOUS STASIS MODEL IN RATS BY HEPARIN AND A VERY LOW MOLECULAR WEIGHT HEPARIN FRAGMENT. RELATIONSHIP TO PLASMATIC HEPARIN ACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644850.

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In this work we investigated the possible relationship between plasmatic activity and antithrombotic activity of a Low Molecular Weight Heparin Fragment (CY222, Choay-Paris) compared with Heparin (Hep). A randomized administration of both test drugs was carried out on 198 rats receiving 4 different dosages (4,2,1 or 0.5 mg/Kg b.w.) or a placebo solution (normal saline). A ligature of the inferior vena cava was performed on rats at T = OH and test drugs were administered subcutaneously at T - 2H. Blood and thrombus samples were taken at T = 6H. For all the tests the Heparin level was computed from a standard curve made up of known amounts of the 3 rd STANDARD HEPARIN (W.H.O.).The statistical study between plasmatic and antithrombotic activities was conducted in 2 steps: 1°) search for linear statistical correlation (correlation factor R, independence test T)For Hep: Thrombin Clotting Time: R = −0.26, T = 0.38, p<0.01; APTT: R = −0.28, T = −2.56, p<0.01; Anti-Xa (chromogenic method CBS 31.39):R = 0.48, T = −4.70, p<0.01; Anti-Xa (Hepaclot, Stago):R = −0.35 T = −3.24, p<0.01; Anti-Xa (Heptest, Haemachem, INC): R = −0.36, T = −3.21, p<0.01; Anti-IIa (chromogenic method CBS 34.47): R = −0.32, T = -2.84, pCO.Ol; For CY222: Anti-Xa (chromogenic method): R = −0.23, T = −1.80, p=0.07; Anti-IIa (chromogenic method): R = −0.26, T = −2.07, p<0.05; 2°) a multivariate regression between thrombus weight (mg) and the plasmatic activity of both the test drugs: For Hep Anti-Xa (chromogenic method): F = 14.56 For CY222 Anti-IIa (chromogenic method): F = 14.40 and Anti-Xa (chromogenic method): F = 5.96.In conclusion, we observe a statistical correlation between Anti-IIa activity and thrombus regression. These parameters may use in human Low Molecular Weight Heparin therapy.
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Yuvenda, Dori, Bambang Sudarmanta, and Arif Wahjudi. "Optimization of CNG injection duration on combustions and emissions characteristics on CNG-CPO biodiesel dual fuel engine with load variations." In THE 4TH BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, HEALTH, AND MEDICAL DEVICES: Proceedings of the International Symposium of Biomedical Engineering (ISBE) 2019. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5138281.

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Kleps, I., A. Bragaru, T. Ignat, M. Miu, M. Simion, F. Craciunoiu, M. Danila, et al. "Nanostructured microcarriers based on silicon for drug delivery." In 2009 International Semiconductor Conference (CAS 2009). IEEE, 2009. http://dx.doi.org/10.1109/smicnd.2009.5336586.

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Reports on the topic "CNS drugs"

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Mery, Laura, Matthew Wayner, John McQuade, and Erica Anderson. Characterization of the Effects of Fatigue on the Central Nervous System (CNS) and Drug Therapies. Fort Belvoir, VA: Defense Technical Information Center, November 2007. http://dx.doi.org/10.21236/ada489794.

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Carroll, David. Targeted CNx Nanowire-Drug Complexes for Enhanced Chemotherapeutic Efficacy. Fort Belvoir, VA: Defense Technical Information Center, September 2009. http://dx.doi.org/10.21236/ada534933.

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Salaymeh, S. R. Scrap Cans Assayed in 55-Gallon Drums by Adapted Q2 Technique. Office of Scientific and Technical Information (OSTI), July 2001. http://dx.doi.org/10.2172/783815.

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Perceptions of community pharmacists, patent and proprietary medicine vendors, and their clients regarding quality of family planning services: The IntegratE Project. Population Council, 2021. http://dx.doi.org/10.31899/rh17.1016.

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The IntegratE Project is a four-year initiative (2017–21) implemented by the Population Council and partners that seeks to increase access to contraceptive methods by involving the private sector (community pharmacists [CPs] and patent and proprietary medicine vendors [PPMVs]) in family planning (FP) service delivery in Lagos and Kaduna States, Nigeria. The project aims to establish a regulatory system with the Pharmacists Council of Nigeria to ensure that CPs and PPMVs provide quality FP services, comply with FP regulations, and report service statistics to the Health Information Management System (HMIS). To achieve this, the project is implementing: a pilot three-tiered accreditation system for PPMVs; a supervisory model to ensure standard drug-stocking practices; building the capacity of CPs and PPMVs to provide a wider range of FP services and data report to the HMIS. This brief focuses on quality of care received by women voluntarily seeking FP services from CPs and PPMVs. CPs and PPMVs and their clients appear to be satisfied with the FP services offered by CPs and PPMVs; on-going learning opportunities, and a supportive supervision system that is properly coordinated should be sufficient to maintain the quality of services offered by CPs and PPMVs.
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